Welcome to How to help ringing ears after a concert!

Medical history, your current and past these abnormalities include hypothyroidism, hyperthyroidism, hyperlipidemia because of the multifactorial nature.

11.06.2015

Symptoms of severe depression and anxiety, treatment for tinnitus caused by hearing loss - Review

Author: admin
Agoraphobia severe depression anxiety disorder Sir Thomas More hard symptoms More harm in severe depression anxiety attacks their day to day lives More upset finding.
The most prominent symptom of major depression is a severe and persistent low mood, profound sadness, or a sense of despair. A variety of symptoms usually accompany the mood change, and the symptoms can vary significantly among different people. Some people who have episodes of major depression also have episodes of relatively high energy or irritability. If a woman has a major depressive episode within the first two to three months after giving birth to a baby, it is called postpartum depression. A depressed person may gain or lose weight, eat more or less than usual, have difficulty concentrating, and have trouble sleeping or sleep more than usual. A particularly painful symptom of this illness is an unshakable feeling of worthlessness and guilt. If pain and self-criticism become great enough, they can lead to feelings of hopelessness, self-destructive behavior, or thoughts of death and suicide.
A primary care physician or a mental health professional usually can diagnose depression by asking questions about medical history and symptoms. Many people with depression do not seek evaluation or treatment because of society's attitudes about depression. There is no way to prevent major depression, but detecting it early can diminish symptoms and help to prevent the illness from returning. Regarding side effects, SSRIs are known to cause problems with sexual functioning, some nausea, and an increase in anxiety in the early stages of treatment. Other effective antidepressants are bupropion (Wellbutrin), venlafaxine (Effexor), mirtazapine (Remeron) and duloxetine (Cymbalta). In the past several years, investigators have raised concerns about an increased risk of suicide in people taking antidepressants. Although experts continue to debate the research, clinicians agree that it is important to have your treatment monitored closely and for you to report any troubling symptoms or worsening mood to your doctor immediately. A number of psychotherapy techniques have been demonstrated to be helpful, depending on the causes of the depression, the availability of family and other social support, and personal style and preference. Depression is a painful and potentially dangerous illness, so you should contact a health care professional if you have any suspicion that you or a loved one is depressed.
When treatment is successful, it is important to stay in close touch with your doctor or therapist, because maintenance treatment is often required to prevent depression from returning. Disclaimer: This content should not be considered complete and should not be used in place of a call or visit to a health professional. The easiest way to lookup drug information, identify pills, check interactions and set up your own personal medication records. Most heart patients will suffer from depression, anxiety, or both at some point along the etiological continuum, and effective treatment of these problems has been shown to improve cardiac outcomes, yet evidence-based treatment for depression and anxiety remains elusive for the vast majority of cardiac patients.
The author, having recently published a patient self-help manual on this topic, calls for emphasis on developing innovative new methods for the treatment of depression, anxiety, and subsyndrome distress for cardiac patients that are effective, rapid, and reasonable in cost. By the year 2020 heart disease is projected to be the number one cause of death worldwide and a particular challenge for India (1).
Studies that focus on women and heart disease are of particular interest because research in both the US (13) and Europe (14) confirms that mortality rates in women patients exceed those in men, even after taking age and comorbidities into account. Prevalence rates for depression among women are higher than rates for men both in the general population (15), and among cardiac patients (16). In sum, the correlation between depression and cardiovascular problems appears to be comparable to the correlation between smoking and CVD (18). These longitudinal studies indicate that depression most frequently occurs before the onset of clinically significant CAD. A range of studies have found high rates of clinically meaningful depressive symptoms among cardiac patients.
When we look prognostically at the risks associated with higher morbidity and mortality for patients with a diagnosis of CVD and depression, we see the mortality rate among clinically depressed patients is quite high and increases with the severity of symptoms and passage of time. A recent study designed to assess the impact of changes in symptoms of depression for heart failure patients found that worsening symptoms of depression were associated with higher rates of cardiac death and cardiovascular hospitalization, even after controlling for baseline depression and established risk factors like HF cause, age, ejection fraction, plasma N-terminal pro-B-type natriuretic peptide level, and prior hospitalizations (44). Studies show that there are several depression-driven biological factors that promote increased morbidity and mortality for people with heart disease (46). Depression also causes increased platelet aggregation (55) and higher platelet monoamine oxidase (MAO) activity, especially in women (56). Research has substantiated the role that chronic stress and depression play in pro-inflammatory processes. Anxiety’s association with CVD has been less well studied than the effect of depression for this population, though the research base is substantial and growing, to such a degree that many researchers in the US have called on the American Heart Association to list anxiety as a major independent risk factor for heart disease. Anxiety is a negative affective state resulting from an individual’s perception of threat, characterized by a perceived inability to predict, control, or gain preferred results in given situations (61). A number of studies have shown that anxiety predicts a higher incidence of cardiac events, higher morbidity and mortality, and poorer quality of life for CHD patients in both the short and long term, independent of conventional risk factors and disease severity (69–71). Anxiety has been shown to predict future coronary events and long-term survival after MI, even after controlling for disease severity and conventional risk factors (79–81). A very large prospective, comparative, cross-cultural investigation by Moser and De Jong was designed to evaluate the impact of anxiety on patient health soon after MI in five countries: Australia, England, Japan, South Korea, and the US (86). Data from the Moser and DeJong cross-cultural study was separately evaluated for gender differences in the presentation of anxiety across culture.
There are several studies which find that anxiety predicts an increased risk of subsequent negative cardiac events for people who already have a diagnosis of CHD.
In a different study by Moser and De Jong, 536 patients with AMI were followed after admission for in-hospital complications (reinfarction, ischemia, ventriculartachycardia, ventricular fibrillation, or cardiac death) (94).
Up to 10% of patients suffer from post-traumatic stress disorder after MI, which interferes substantially with treatment compliance and leads to extremely poor outcomes (95). The biophysical mechanisms whereby anxiety may contribute to the onset of CHD and negative CHD outcomes appear to be several and, as with depression, chiefly focus on the role of the SNS. It has been found that patients with GAD have lower vagal tone than those with low levels of anxiety, which allows SNS activity to predominate (101,102).
Cardiovascular reactivity (CVR) is exaggerated in people with anxiety so that stressful stimuli can produce frequent, pronounced, and sustained changes in blood pressure, heart rate, stroke volume, and total peripheral resistance, which may then contribute to the etiology of heart disease and poor prognosis (104). Stress-induced ischemic events may occur at relatively low heart rates, and as many as two-thirds of these events may go unnoticed by patients (119). Patients with AMI who were exposed to mental stress testing experienced increased platelet aggregation, formed more circulating platelet aggregates, and developed higher plasma and serum thromboxane B2 levels than healthy controls (123).
Several studies have examined the incidence rates for diagnosable depression and anxiety among patients waiting for heart transplant. Substantial research has focused on the role that certain personality types have in the etiology and prognosis of CVD: specifically type A and type D personalities.
Type A behavior pattern (TABP) or type A personality, first researched in the 1950s, is characterized by anger, hostility, impatience, a chronic sense of time urgency, excessive competitiveness, undue ambition, and social timidity. An early study by Denollet and Brutsaert followed patients for a mean of 7.9 years after MI using the Millon Behavioural Health Inventory, with the purpose of investigating the association between type D personality and mortality after MI.
Heart patients who suffer from subsyndromal mental distress are more prone to thrombogenesis, arrhythmogenesis, altered heart rate variability, increased platelet aggregation, increased myocardial oxygen demand, myocardial ischemia, impaired ventricular function, and cardiac dysrhythmias (138–140).
These research findings, taken collectively, indicate that subsyndromal mental distress poses a significant threat to heart health for the general population and is particularly toxic to patients who already have a diagnosis of CVD. Research shows that depression is a known cause or correlate of many of these established psychosocial and behavioral risk factors, namely less exercise, poor diet, obesity and smoking, especially in women (148), failure to use social support resources (149,150), and triple the risk of noncompliance with physician-ordered medical regimens (151). Chronic stress, depression, and anxiety, to varying degrees, are factors in the onset and severity of diagnoses that frequently co-occur with or presage CVD: hypertension, metabolic syndrome (MetS), and diabetes.
There is a substantial research base, nearly a century in the making, linking hypertension to negative affect, anxiety, depression, stress in general, and negative personality traits. Depression and distress are associated with MetS in the research literature, though more research needs to be done on this association.
In another study by Skilton et al., 1,598 subjects at risk of CVD were assessed for metabolic syndrome, depression, and anxiety to investigate whether metabolic syndrome is associated with anxiety or depression, whether these relationships vary by gender, and whether they are independent of age, obesity, smoking status, socioeconomic factors, and lifestyle (172). Chronic stress is now believed to be the leading cause of depression (173) and acute stress, especially if it is encountered in childhood, the most significant factor in the development of anxiety disorders and depressive disorders later in life (174). Science long ago proved that stress is actually necessary and helpful to our evolution as a species. Equally well-researched are the serious neuropsychiatric and health consequences of repeated exposure to acute stress.
Chronic psychosocial stress is a known factor in the etiology and course of CVD but is often dismissed in clinical settings. Chronic stress has been shown to sustain HPA hyperactivity even in the absence of current stressors, increase production of corticoids, cause neuronal death, reduce hippocampal size and density, alter feedback pathways in the brain, lower levels of serotonin, and reduce levels of brain-derived neurotropic factor (181–183). More than a dozen potential biomarkers that interact with stress to promote the etiology of clinical depression and anxiety have been identified, including monoamine regulators, proinflammatory cytokines, and other inflammatory mediators, mediators of glutaminergic activity, and GABAergic activity, as well as regulators of neurogenesis (186). Table 1 provides list of the most common symptoms of stress and Table 2 the list of clinical criteria for depression and anxiety. People who have four or fewer symptoms from the checklists in Table 2 are considered subsyndromal, regardless of symptom severity. Anxiety and depression have symptoms in common but overall their symptoms exhibit distinct central tendencies: anxiety is usually accompanied by excessive, exaggerated worry about everyday events and hyperactivity, while depression tends to be dominated by feelings of sadness, guilt, lack of self-worth, in-activity, and withdrawal.
Research evidence suggests genetic and neurobiologic similarities between depressive and anxiety disorders, many of which have been reviewed in this article. It should be noted that a substantial number of patients satisfy full diagnostic criteria for both depression and anxiety, evidencing true comorbidity.
Frasure-Smith and Lesperance assessed the prognostic importance of MDD and GAD together with self-reports of anxiety and depression and their co-occurrence during 2-year follow up of 804 men and women with stable CAD, measuring incidence of major adverse cardiac events or MACEs (cardiac death, MI, cardiac arrest, or nonelective revascularization) in the 2 years following baseline (197).
It is remarkable that depression, in and of itself without any specific comorbidity, is associated with a decrement in health status almost as bad as the decrement associated with congestive heart failure after each group is adjusted for the presence of comorbidities (200).
Mental problems are grossly under-reported owing to the stigma associated with mental illness, and this is especially true for India, whose honorable, dutiful, intelligent populace tends to view mental instability as a personal failure.
While there are no reliable nationwide data on rates of anxiety in India, limited data from the WHO place the current point-prevalence rate of GAD at 8.5% (206).
The escalating incidence of mental illness in India is a function of several economic and cultural factors.
The Regus Work-life Balance Index for 2013, which surveyed more than 26,000 professionals in more than 90 countries, ranked India second-worst in the world (second only to Mexico) for poor work–life balance, high rates of work-related stress, and frequency of stress-related illness (209).
Increasing rates of chronic stress, distress, depression, and anxiety in India should be of great concern from both the clinical and public health perspectives.
Depression, anxiety, and distress in the cardiac patient can be treated effectively, even cured, resulting in vastly improved cardiovascular health and reduced risk of future adverse cardiac events and lower utilization of costly health and allied health services (212).
Institutions that specialize in integrative medicine, like The Benson-Henry Institute of Mind-Body Medicine at Massachusetts General Hospital (the number one-ranked hospital in the US) have established the remarkable effectiveness of mind-body medicine in the treatment and prevention of heart disease and other stress-related illnesses. It won’t be lost on the reader that the basic tenets of mind-body medicine are analogous to those of the yogic lifestyle, which is highly effective in the prevention and treatment of heart disease, chronic stress, and stress-related illnesses. In recognition of a growing body of research evidence demonstrating the effect of the mind on bodily health, the field of clinical psychology developed a specialty called Health Psychology, and in 1977 health psychology became a division of the American Psychological Association. CVD is a multifactor problem that requires a multifactor solution, and the same is true for depression, anxiety, and subsyndrome distress. Cardiologists and other medical specialties, as well as doctors who work in primary care settings, are generally not eager to function in the role of a mental health professional, nor do they have the time and resources. In 2008 The American Heart Association published physician guidelines for the diagnosis and treatment of depression in heart patients (221). Not at all (score 0), Several days (score 1), More than half the days (score 2), Nearly every day (score 3). Given the popularity of the two-stage PHQ series for assessing and monitoring depression, similar 2- and 7-step anxiety screeners were developed by Spitzer et al. The patient responds using the same 4-point scale used in the PHQ: Not at all (score 0), Several days (score 1), More than half the days (score 2), Nearly every day (score 3). The underdiagnosis of depression in cardiac care is highly significant, greater even than in primary care settings, where doctors fail to diagnose depression more than half the time. Studies have shown that the symptomology of depression in cardiac patients often differs from that observed in general psychiatric patients.
In the majority of cardiology practices in the US, a cardiac patient with positive screening results for depression, anxiety, or distress is referred for evaluation to a mental health professional who is qualified in the diagnosis and treatment of these disorders.
Ideally, treatment of depression and anxiety in cardiac patients should be based on a differential diagnosis of patient need within the larger framework of mind-body medicine, using a multifactor approach, and treatment should be formulated using evidence-based modalities. Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs), Serotonin Antagonist and Reuptake Inhibitors (SARIs), and benzodiazepines are considered the prescriptive choice for people with depression and anxiety in the general population. In the majority of cardiac settings, treatment for depression and anxiety is still mostly limited to the dispensing of SSRI medications, despite their limitations and recent challenges to their efficacy. There is some evidence that SSRIs may improve depressive symptoms and reduce the frequency of reinfarction and death due to MI for extremely depressed patients with CAD, but they do not render these benefits with consistency.
In the Canadian Cardiac Randomized Evaluation of Antidepressant and Pychotherapy Efficacy (CREATE), 284 patients with chronic CHD and MDD (a score of 20 or more on the 24-item HAM-D) were randomly assigned half to the SSRI citalopram, and half to placebo. Apart from questions regarding efficacy and reliability, SSRIs have mild cardiotoxic effects, to include increased heart rate and reduced heart rate variability (252) and they alter the activities of cytochrome P450 (CYP) liver enzymes involved in the metabolism of drugs frequently prescribed for heart patients, including but not limited to β-blockers, warfarin, type1 antiarrhythmics, and calcium antagonists (253). In the hands of a properly trained doctoral-level clinician, psychotherapy can reverse the neurobiologic and psychological consequences of chronic stress, depression and anxiety, is preferred over medication therapy by many patients, and can be combined with medication to increase medication efficacy in patients with more severe psychiatric diagnoses (260). Along with medication therapy, CBT was used in ENRICHD (261), IPT was used in CREATE (262), and problem-solving therapy in the Coronary Psychosocial Evaluation Studies (COPES) (263,264). Psychotherapy works well to improve the health and longevity of cardiac patients, but the resources (human and financial) needed to provide it at sufficient levels of intensity are typically only available for the upper classes. There are many forms of CBT, all of which focus on changing distorted thought patterns that are driving harmful emotion and dysfunctional behavior, creating effective strategies for overcoming problems, generating self-efficacy and self-esteem, building the patient’s internal locus of control, and reducing mental and biological stress (274,275). IPT is an empirically validated treatment proven effective for clinical depression, social phobias, majoranxiety disorder, bipolar disorder, and post-traumatic stress disorder (276,277). The mood changes that occur in major depression are defined as lasting at least two weeks but usually they go on much longer — months or even years. Some people who have many episodes of major depression also have a background pattern of a milder depressed mood called dysthymia.
They may sleep far less than normal, and may dream up grand plans that could never be carried out. Depression that occurs mainly during the winter months is called seasonal affective disorder, or SAD.


The vast majority of people who suffer severe depression do not attempt or commit suicide, but they are more likely to do so than people who are not depressed. By definition, major depression is diagnosed when a person has many of the symptoms listed above for at least two weeks. The person may feel the depression is his or her fault or may worry about what others will think. The older classes of antidepressants, tricyclic antidepressants and monoamine oxidase inhibitors, are still in use. Once the right medication is found, it may take up to a few months to find a proper dose and for the full positive effect to be seen. Or a mood stabilizer, such as lithium (sold under several brand names) or valproic acid (Depakene, Depakote), is added. A technique called cognitive behavioral therapy is designed to help a depressed person recognize negative thinking and teaches techniques for controlling symptoms. This material is provided for educational purposes only and is not intended for medical advice, diagnosis or treatment. According to WHO statistics India has the highest rate of CHD among developing nations and experiences more than twice the rate of death per 100,000 population due to CHD as the United States (2).
Depression and depressive symptoms are also associated with 2–3 times higher mortality rates for patients with stable CAD and for those who suffer myocardial infarction (MI), unstable angina, and coronary artery bypass.
Clearly, a diagnosis of CVD, the physical degradations and disabilities associated with it, and the stress of medical procedures and surgery, are significant enough to cause or exacerbate depression in people with heart disease. One authoritative study by Denollet and Brutsaert placed the incidence rate of clinical depression among cardiac patients as high as 50.5% (19). The relative risk ratio for death within 6 months among post-MI patients with MDD, versus post-MI patients without depressive disorder, was reported as 3.1 by both Schleifer at al.
It is well-established that depression is associated with higher rates of healthcare utilization and costs for all heart patients (45). Depression is associated with alterations in immunological functioning relevant to pro-inflammatory processes.
There are several different subtypes of anxiety, including panic disorder, social anxiety disorder, generalized anxiety disorder (GAD), simple phobia, obsessive-compulsive disorder, and post-traumatic stress disorder. Studies among initially healthy individuals who were followed to detect the occurrence of CHD report a range of prognostic risk factors based on the population under study, outcomes measured, and duration of follow up. The Normative Aging Study, a large prospective study conducted in Boston, found that higher levels of worry (a key symptom of anxiety) were found to predict increased risks of both MI and fatal CHD in male subjects at 20-year follow up (66). Persistent anxiety predicts worse disability, more physical symptoms, and poorer functional status in CHD patients (72,73). Anxiety post MI is also associated with increased in-hospital complications such as lethal dysrhythmias, continued ischemia, and reinfarction (82), longer stays in the cardiac care unit and hospital (83)[, more frequent and severe symptoms, regardless of the severity of a patient’s physical condition (84), higher consumption of healthcare resources, and lower quality of life post-discharge (85).
Overall, women reported mean anxiety levels 25% higher than those reported by men – a pattern of higher anxiety in women that was seen in each country studied, which (according to the study authors) may account for poorer prognosis seen in women post-MI (88). This study found that patients with high anxiety had twice the occurrence of complications as patients with low anxiety, independent of age, diabetes, previous AMI, type of AMI, and Killip class.
Anxiety, both episodic and chronic, contributes to excessive activation of the SNS, and release of epinephrine, norepinephrine, and cortisol. Research has also shown that anxiety can lead to increased blood cortisol levels that promote elevated resting blood pressure and heart rate (103). Magni and Bogherini (126) found that 35% of patients waiting for heart transplant suffered from anxiety disorders and more than 20% suffered from marked depressive symptoms.
Type A personalities have been shown to have twice the risk for onset of CHD and higher rates of morbidity following diagnosis when compared to people of normal temperament and mood (131).
Type D people are often worried without specific reasons, often feel depressed and irritated, and rarely experience positive feelings. The relative risk of cardiac death in patients with type D personality versus patients asymptomatic for depression and anxiety in this study was 4.3 (133). MSI, covered previously in this article, is driven by fairly low levels of anxiety and nervousness typical for the general population, yet has disastrous consequences for the heart patient.
It is well-documented that the incidence of chronic stress, depression, and anxiety is higher among people of lower socioeconomic status (146).
Anxiety, both clinical and subclinical, is also associated in the research literature with behaviors that are contraindicated for a healthy heart.
This study concluded that metabolic syndrome is associated with depression and depressive symptoms, but not statistically significantly associated with anxiety, irrespective of gender, and obesity in subjects at risk for CVD.
Recent research in humans shows that cumulative exposure to adverse life events is associated with smaller gray matter volume in key prefrontal and limbic regions of the brain involved in stress, emotion and reward regulation, and impulse control (175). For example, there is a large body of research evidence linking combat stress with persistent HPA hyperactivity, reductions in functional connectivity between the midbrain and prefrontal cortex, and significant impairment to memory and cognition, all of which are markers for post-traumatic stress disorder (177), which is very highly correlated with the etiology of CHD and high rates of CHD-related morbidity and mortality (178). On observation, the symptoms for depression and anxiety are nearly identical to the symptoms of stress.
Subsyndromal depression and anxiety is very frequently seen in patients with heart disease and, as previously cited, these distressed patients are more than twice as likely to develop CVD and up to three times more likely to have a poorer prognosis than patients with normal mood (190).
It is quite common for patients with clinical depression to have symptoms from the anxiety checklist and vice versa. They found that anxiety and depression both predict greater MACE risk in patients with stable CAD. Physical function and general health are also lower for depressed patients compared to patients with other chronic diseases such as diabetes and CAD. Unfortunately, high rates of chronic and acute stress, a cultural disdain for seeking help with mental problems, and a lack of early intervention and treatment alternatives have combined to fuel an epidemic of depression and anxiety in India. According to the National Crime Records Bureau of the Indian Ministry of Home Affairs, 135,445 people committed suicide in India in 2013 and of these, 68% were between the age of 15 and 29 (205).
Senior fellows at the National Institute of Mental Health and Neurosciences estimate the point prevalence for anxiety disorders to be 20–25%, or one out of every four or five Indians (207).
In this survey, respondents labeled work problems, personal finances, commuting to work, and instability in the world economy as the chief reasons for their increasing stress. Research shows that psychosocial risk factors for mental illness that disproportionately affect women include gender-based violence, socioeconomic disadvantage, low income and income inequality, low or subordinate social status and rank, and responsibility for the care of others (210).
Jon Kabat-Zinn in the US developed the MBSR, a mindfulness-based stress reduction program involving mild forms of Hatha Yoga in combination with meditation, exercise, and a healthy diet, which demonstrated statistically significant levels of stress-reduction, positive changes in brain activity, improved emotional processing, better immune functioning, better circulation, and other symptom reduction in people who suffer from heart disease and breast cancer (217,218). To answer this challenge, a great deal of research has been devoted to depression and anxiety screening instruments that are valid, specific, and brief.
It suggested the use of the two-question Patient Health Questionnaire, or PHQ-2 for use in busy primary and specialty healthcare settings.
Despite its brevity, the PHQ-9 provides the sensitivity and specificity needed for assigning a provisional diagnosis of depression. Complaints of tiredness or lack of energy are more frequent for people who suffer from heart disease and depression, whereas melancholy or depressed mood states are more common for psychiatric patients in general (230–232).
The modalities which have been demonstrated effective for this population are pharmacotherapy, psychotherapy, clinical hypnosis, meditation, exercise and somatic relaxation techniques, support groups, cardiac rehabilitation, and case management.
Of these, safety for heart patients has been examined in clinical trials for fluoxetine and sertraline (236–238), citalopram (239)[2, and mirtazapine (240). Recent research, reviewed in prior sections of this article, shows that serotonin depletion is but one of multiple neurobiologic effects of chronic distress, depression, and anxiety. Depressed patients who received sertraline experienced fewer severe adverse cardiovascular events (another MI, stroke, or death) during follow up than depressed patients in the control group. Citalopram showed antidepressant efficacy (reduction of depressive symptoms) in some patients and no evidence of harm, but also failed to show any statistically significant improvements in cardiovascular health for study participants (251). Following AMI especially, patients taking anticoagulant therapy and SSRIs run a higher risk of bleeding (254). Based on research evidence, tricyclic antidepressants (TCAs) are specifically contraindicated for heart patients because they can produce quinidine-like cardiotoxic effects that include QTc prolongation, conduction delay, block of the A-V conjunction and bundle branches, bradycardia, tachycardia, atrial or ventricular arrhythmia, cardiac arrest, ST-T abnormalities, MI, and exacerbation of heart failure (255,256). Cardiac arrhythmias and QT prolongation have been reported with SARI use and they are specifically contraindicated for patients during the initial recovery phase following MI (257).
In all these trials, patients suffering from CHD and psychological disorders experienced treatment efficacy (remission of psychological symptoms) but little statistically meaningful reduction in coronary morbidity and mortality. Indeed, the chief reason there is little research basis for the efficacy of psychotherapies in cardiac patients is that their use is limited by the lack of mental health professionals with specialized training in cardiac psychology and limits on the financial resources needed to sustain clinically meaningful levels of intervention (269). The American Psychiatric Association practice guidelines state that CBT and interpersonal psychotherapy (IPT) have the best-documented efficacy for treatment of MDD and anxiety disorders (271,272). It has been studied extensively and proven effective with individuals and families experiencing chronic and acute stress and distress (280–282). The psychological distress of each partner and the couple’s adjustment in dealing with CHD plays a substantial role in patient recovery from significant cardiac events. Treatment Treating mixed anxiety depressive trouble can be difficult for physicians because about treatments are more luckily treating economic crisis also helps ease symptoms of anxiety. Or the person suffering major depression may not be able to take pleasure in activities that usually are enjoyable. The person may develop thinking that is out of step with reality — psychotic symptoms — such as false beliefs (delusions) or false perceptions (hallucinations). People who have a family member with major depression are more likely to develop depression or drinking problems. They include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil) and citalopram (Celexa).
They are as effective as the newer ones and can be very useful when someone has not responded well to other treatments.
Psychodynamic, insight-oriented or interpersonal psychotherapy can help depressed people to sort out conflicts in important relationships or explore the history behind symptoms.
In ECT, an electrical impulse is applied to the person's scalp and passes to the brain, causing a seizure.
On this basis the American Heart Association listed depression as a major independent risk factor for heart disease in February of 2014 and strengthened its guidelines for the screening and treatment of depression in people with heart disease. However, SSRI’s show clinical effect less than half the time, have recently been shown to be no better than placebo, and have mild cardio-toxic effects. Remarkably, these correlations held after adjustment for conventional prognostic risk factors like smoking, hypertension, and obesity (5).In one of the earliest longitudinal studies ever conducted, all male medical students who entered The Johns Hopkins Medical School from 1948 to 1964 were followed annually until the study results were reported in 1998 (6).
The wide range of risk across studies is associated with different scales used to measure depression and subsyndrome depressive symptoms, great variation in study length, and substantial difference in study cohort characteristics (age, gender, socioeconomic status, diagnosis). The incidence and severity of depression were evaluated according to the Zung Self-Rating Depression Scale (SDS). This study found that, after multivariate adjustment for traditional CAD risk factors, depressive symptoms predicted CAD severity and increased risk of death in women 55 and younger, but not in men 55 or younger, nor in women over the age of 55. They found that CHF patients who met DSM-IV criteria for major depression had a mortality rate more than twice that of those who were not depressed, and three times as many hospitalizations. High levels of cortisol are known to redistribute body fat and increase the risk of heart disease (47).
Specifically, depression has been associated with an elevation of interleukin-6 (IL-6), a primary pro-inflammatory cytokine (59,60).
Anxiety disorders can evolve as a normal reaction to chronic stress and cumulative adversity, and acutely stressful situations (like having an MI) can trigger anxiety. Weissman followed 3,778 healthy men and women for the incidence of acute MI and found the probability of AMI in anxious people was 4.5 times as high as risk of AMI in nonanxious individuals (63).
It hinders patient self-care abilities post MI (74,75),[7 retards patient ability to implement needed lifestyle changes (76)[, and lowers adherence to physician-ordered rehabilitation efforts (77).
The authors concluded that patients suffering MI display a similar emotional response to this potentially life-threatening event, regardless of country of origin and culture. Rates of anxiety in the general population are higher for women than for men, and women tend to suffer higher anxiety than men post-MI, a finding that is consistent across a variety of Western and Asian cultural groups (89). Evidence suggests that both epinephrine and norepinephrine function as platelet agonists (96) and that epinephrine accelerates hemostasis and fibrinolysis (97). Mental stress increases heart rate and negatively affects the balance between myocardial oxygen supply and demand (107). In a review article, von Kanel concluded that patients with atherosclerosis who experience anxiety and mental stress may tend toward hypercoagulation due to endothelial dysfunction and reduced fibrinolysis (125).
Their etiological risk for CHD is estimated to be twice as high as that for people with normal temperament and mood, and their relative risk of cardiac death following the onset of CHD almost three times higher (132). Those with anxiety are more likely to eat an unhealthy diet, smoke, use drugs or alcohol or both, fail to adhere to physician instructions, experience sleep disturbance, and be physically inactive (152–154). Both chronic physical and emotional stress, especially chronically negative emotion, increase levels of cortisol and epinephrine, which can result in elevated blood glucose levels and greater insulin resistance. This relationship remained after controlling for age, race, education, smoking, physical inactivity, carbohydrate consumption, and alcohol use. Older women showed the same pattern but less severe, and older women using hormone replacement therapy (HRT) did not show this pathway. However, it is important to draw a clinical distinction between ordinary stress, known as eustress in the scientific literature, and distress.
Rohleder concluded that repeated psychosocial stress causes and sustains low-grade systemic inflammation, which plays a key role in the pathophysiology of CVD, and further, that lower subjective social status and perceived limits surrounding pursuit of purpose in life are associated with increased inflammatory responses to repeated stress exposure (184). Study participants were regularly interviewed for stress symptomology and received CT examinations in 1968, 1974, 1980, 1992, and 2000. This study found that teenage boys who had some depressive symptoms at the start of the study, together with high levels of circulating morning cortisol (as measured in their saliva) were 14 times more likely to develop major depression within the following 3 years than boys without any signs of depression and low levels of cortisol, and 2–4 times more likely to develop clinical depression than boys with either depressive symptoms or high levels of morning cortisol.
In this study, researchers found the SKA2 mutation was associated with higher levels of cortisol and glucocorticoids and significantly interacted with chronic stress and anxiety to explain about 80% of suicidal behavior and progression from suicidal ideation to suicide attempt (188). The difference between stress symptomology and the clinical criteria for a psychiatric diagnosis lies primarily in symptom volume and chronicity. Approximately 85% of patients with depression also have significant symptoms of anxiety, an association that holds true for men in the particular, and significant depressive symptoms occur in up to 90% of patients with anxiety disorders (192,193). This study found that younger age at onset of HF and depressive symptoms were independent predictors of anxiety (199). The excessive morbidity associated with depression is well-documented in the scientific literature, but its implications have been largely ignored by mainstream medicine until recently, owing to unprecedented increase in rates of depression, anxiety, and distress worldwide. Suicide is the third leading cause of death among teenagers worldwide, following accidents and AIDS.
India is now considered to be the stress capital of the world, eclipsing even Japan and the US for this dubious honor.
Mind-body medicine combines clinical therapies and healthy lifestyle elements to reverse the genetic, biophysical, and mental determinants of illness, foster superior mental and physical health, and create resilience to stress and stress-induced illnesses.


Herb Benson, founder of the Benson-Henry Institute and considered to be the father of mind-body medicine in the US, is a cardiologist who pioneered meditation research for its healthful effects on the cardiovascular system in the 1970s (213,214).
It appears that health psychology’s association with each major disease is characterized by unique and specific theoretical and methodological characteristics, and there is debate in the field of medicine as to whether these subspecialties should be considered part of clinical psychology or as new, autonomous medical disciplines (219).
The PHQ-2 is self-administered by the patient and can be scored by a nurse or admitting staff member. A score of 3 or more has been shown to have a sensitivity of 83% and a specificity of 92% for major depression (222)[2; 3 is considered the optimal cut-point for further screening and a score of 0 virtually excludes depression. It also provides a severity measure for treatment planning purposes, serves as a diagnostic instrument for the depression criteria listed in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (the DSM IV), and it has been proven accurate for patients with CAD (224,225).
This series is called the GAD-2 and GAD-7, respectively, with GAD meaning generalized anxiety disorder . A score of 3 or higher warrants assessment with the GAD-7, which provides severity measures across all 7 diagnostic criteria for anxiety in the DSM IV. In the meantime, the PHQ and GAD screeners yield valid results and can be administered with little or no staff time and resources.
Many doctors are reticent to screen for mental disorders if they have no reliable resources for patient referral and treatment for these problems. SSRIs work on average less than 50% of the time and when they do work, efficacy can range from almost no effect to the remarkable, showing tremendous variance among individuals, hospitals, and clinics. An SSRI, while a helpful adjunct to the treatment of depression, major depression especially, does not target the most frequent underlying cause of depression: mental distress and stress-related neuroendocrine pathology. Patients with depression were randomized into a protocol that included low-intensity cognitive behavioral therapy (CBT) (6 individual and group sessions over 11 weeks). However, based on small sample size (369 patients) and short duration of follow up, it is not possible to generalize these findings (249).
Although benzodiazepines have long been prescribed for short-term use by the post-MI patient to reduce anxiety, there are no controlled trials documenting the benefits of this protocol (258) and recent research suggests that sustained use of benzodiazepines may contribute to heart failure and cardiac death (259). Problem-solving therapy and relaxation therapies are also proven adjuncts to treatment for depression and anxiety, and in heart patients, emotionally focused therapy (EFT) for couples and families has been shown to improve cardiac outcomes (273).
Couple quality has been found to moderate the relationship between stress and wellness, acting as a protective factor in emotionally healthy couples, or increasing vulnerability to illness for at-risk patients who are in emotionally unhealthy relationships (283).
Levels of psychological distress in both partner and patients have been identified as significant, with 57% of patients and 40% of partners meeting criteria for a psychiatric disorder following a major cardiac event (288).
Ascertain how the symptoms of impression anxiety disorder and bipolar shifts in severe depression anxiety attacks a person's modality from severe impression to manic phases with soaring highs.
Therefore family members or friends may need to encourage the depression suffer to seek help.
They are not without problems, but they are fairly easy to take and relatively safe compared with previous generations of antidepressants.
But a very small number of people taking these medications probably do have an unusual reaction and end up feeling much worse rather than better. These include haloperidol (Haldol), risperidone (Risperdal), ziprasidone (Geodon), aripiprazole (Abilify) and olanzapine (Zyprexa, Zydis). Psychotherapy and clinical hypnosis have proven effective but can take too long, can be costly, and are difficult to provide in cases where properly trained doctoral-level clinicians are lacking.
Gupta showed that CHD is responsible for 40% of urban deaths, 30% of deaths in rural areas, and growing at a phenomenal rate, increasing in urban areas from 1960 to 2000 by more than 500%, and in rural areas from 1970 to 2000 by nearly 250% (3). Depressive symptoms were scaled from 0 to 4, with a grade of 2 or higher equivalent to clinical depression.
According to this study, the higher the SDS score, the higher the risk of cardiac death and all-cause mortality.
The authors conclude that younger women may be especially vulnerable to the adverse cardiovascular effects of depression (35). They also found the relationship between depression and higher rates of mortality and re-hospitalization was independent of advanced age and severity of ischemic etiology of CHF.
These risk ratios were independent of age, New York Heart Association class, baseline ejection fraction, and ischemic etiology of CHF. Although smoking and ventricular arrhythmias are more common in depressed patients, depression adversely affects the course of heart disease independent of these factors (58).
In a similar study of 2,280 community dwelling men with a 32-year follow up, the rate of sudden death due to heart disease was 4.46 times higher for anxious individuals than for those without anxiety.
For patients with low perceived control, 20% experiencing low anxiety versus 80% experiencing high anxiety experienced complications.
Patients with CHD and elevated anxiety or prolonged stress and a history of AMI have higher plasma norepinephrine levels (98). High anxiety is also associated with prolonged QTc intervals, and has been shown to increase risk for lethal cardiac dysrhythmias (106). Patients with higher levels of norepinephrine had more ischemic episodes, and their ischemic episodes lasted longer (122).
Independent studies also suggest that psychological stress is a strong determinant of behavioral risk factors that contribute to the onset of hypertension and its maintenance, to include smoking, obesity, poor diet, substance abuse, and physical inactivity (157–159).
In this survey, men with a history of depression were not significantly more likely to develop MetS. This phenomenon is well-known in the disciplines of clinical psychology, neuropsychology, and psychiatry and substantial current research is focused on strategies to prevent or reverse the detrimental effect of early life stress on the CNS. This study found that women who reported frequent or constant distress at one or more examinations in 1968, 1974, or 1980 developed moderate-to-severe white matter lesions and moderate-to-severe temporal lobe atrophy by 2000 (185). Girls with some depressive symptoms and high levels of cortisol were 4 times more likely to develop major depression within 3 years than same-age girls who had no symptomology and low cortisol levels at the start of the study (187).
At least five of the symptoms on the Table 2 checklists must be present nearly every day, most of the time, in order to make a diagnosis of clinical depression or anxiety. Although depression and anxiety symptoms co-occur with great frequency and they share a substantial component of general affective distress, they can be differentiated based on factors specific to each syndrome (194).
By and large these patients have a more protracted course of illness and respond less well to therapy (196).
The World Health Organization (WHO) estimates that, owing to the rise of chronic stress globally, depression has become a pandemic.
In this study, the incidence of depressive episodes was higher for women than for men by a ratio of 2:1, which also holds true in the US (203). In pursuit of superpower status and lifestyle, a majority of Indian companies and employees are making unhealthy tradeoffs. In addition, the yoga group showed greater reduction in BMI, waist circumference, LDL-C, and systolic blood pressure (215). Like the PHQ-2, it is self-administered by the patient and can be scored in moments by a nurse or staffer. Like the PHQ series, the GAD screeners are patient self-administered and can be scored by a nurse or staffer in moments. Recent research has provided clarity on this dilemma, however, and the evolving consensus among medical professionals is to screen patients as early as possible, regardless of whether mental health treatment options are available. The AHA recommends, based on research evidence, that patients with heart disease who are being treated for depression (and anxiety) should undergo careful monitoring for adherence to their medical treatment regimen, and for the efficacy and safety of drug therapy for their medical and mental health conditions (235). For all these reasons, the standard of practice for major depression requires both psychotherapy and anti-depressive medication to be administered. Patients who showed less than a 50% reduction in Beck Depression Inventory scores after 5 weeks of CBT were referred to a psychiatrist for pharmacotherapy, usually sertraline.
Indeed, subsequent analysis of data from SADHART showed that treatment with sertraline compared with placebo did not support improved cardiovascular status among patients with depression at statistically significant levels (250).
The Recurrent Coronary Prevention Project, in which 1,013 MI patients with depressive symptoms were randomly assigned to receive psychotherapy and social support, showed a reduction in depressive symptoms and a 44% reduction in cardiac death and nonfatal MI for the treatment group (268).
Couple conflict has been associated with increased blood pressure (284) and high levels of catecholamines and stress hormones (285). Researchers have suggested that this is an expression of empathy: the more couples love and rely on one-another, the more they find a significant cardiac event stressful (289). If a person has milder symptoms of mania and does not lose touch with reality, it is called "hypomania" or a hypomanic episode. Meditation has been proven effective in the treatment of coronary artery disease (CAD) and for mild to moderate depression and anxiety but most cardiac patients quit its practice before it can deliver clinical benefit, and it is not effective as a stand-alone intervention for moderate to major depression and anxiety. The definition of CAD included MI, angina pectoris, chronic heart disease, and other types of symptomatic disease that required coronary artery bypass surgery or percutaneous transluminal coronary angioplasty. In this study, patients with major depression had a 4.5-times higher risk of experiencing a heart attack (MI) during a 13-year follow up than those without major depressive disorder (MDD). In this study, the higher the depression grade, the greater the incidence of morbidity and mortality due to heart-related pathology. Patients who were moderately to severely depressed had a 69% higher risk of cardiac death and 78% higher risk of all-cause mortality when compared to patients without depression. Research strongly suggests that anxiety at every step along the continuum has comparable cognitive, neurobiological, and behavioral effects, and that clinical and subclinical anxiety are not fundamentally different phenomena – both have dilatory effects on patient health (62). Legault and colleagues reported that 49% of the patients they examined experienced stress-induced ischemia, patients with more severe coronary artery stenosis were the most likely to experience stress-induced ischemia, and stress-induced ischemia is often silent (116). Research suggests that patients 40 years of age and older who experience hyperglycemia in response to acute stress are more likely to develop type 2 diabetes in subsequent years (161). Depressed diabetic patients have been shown to have higher ambulatory care use, fill more prescriptions, and utilize up to 4.5 times as many financial resources for their treatment than nondepressed diabetic patients (164).
MetS was associated with a current diagnosis of major depression and overeating, but not with age or sex (169).
By contrast, distress is a harmful, intense emotional and biological stress reaction that does not resolve without significant intervention and persists even in the absence of current stressors. The study authors found that higher SLE and higher social strain were associated with a higher incidence of CVD and hemorrhagic stroke, independent of sociodemographic factors and depressive symptoms (180). Patients who meet these criteria are then assessed for symptom severity to determine whether their clinical presentation is mild, moderate, or severe. This study found that anxiety symptoms were the strongest predictor of future negative cardiac events, rehospitalization, and increased healthcare consumption for men (198). Doctors from The National Institute of Mental Health and Neurosciences and leading psychiatrists in private practice report that the incidence of depression is rising precipitously, especially in urban areas, where the current point prevalence of depression among Indians is estimated to be 10% (204).
Scores of 5, 10, and 15 represent cut-points for mild, moderate, and severe anxiety respectively. These findings are startling given the low frequency and intensity of psychosocial intervention typically employed in randomized trials. Conversely, pre-MI marital happiness is consistently associated with lower levels of stress in patients following MI and better health outcomes (286).
A patient’s wellbeing in their primary relationship has been found to be a powerful predictor of recovery from a cardiac event (290) and relationship problems that existed before a cardiac event have been shown to worsen after a cardiac episode (291).
And genetic makeup influences how vulnerable any of us is to breakdowns in these functions. The cumulative incidence of clinical depression in this cohort of 1,190 participants at 40 years of follow up was 12% (lower than the incidence of depression in the general population). Patients with depressive symptoms that fell below the clinical criteria for major depression were twice as likely to die of MI as patients with no depressive symptoms whatsoever. A high depression grade correlated with an almost threefold increase in risk for angina pectoris. Patients who were mildly depressed had a 38% higher risk of cardiac death and a 57% higher risk of all-cause mortality when compared with nondepressed patients. In all these studies, anxiety was found to predict subsequent cardiac events independent of conventional risk factors and disease severity. Mental stress has also been shown to induce wall motion abnormalities and decreased LV ejection fraction in CAD patients (117). Major depressive episodes were the most frequent psychiatric disorder, followed by anxiety disorders.
Chronic stress and acute stress induce the neurobiologic changes that lead to distress, depression, and anxiety. When screening for anxiety disorders, the recommended cut-point for further evaluation is a score of 10 or greater, which has a sensitivity of 89% and specificity of 82% for GAD. Follow-up interview data on patient use of antidepressants and counseling were collected at 1 and 6 months but otherwise the cardiac care team was uninvolved in mental health service delivery or case coordination. ECT is the quickest and most effective treatment for the most severe forms of depression, and in most people, it is not more risky than other antidepressant treatments. In this study, clinical depression was associated with a more than twofold higher risk of later CAD. Subclinical, fairly common depressive features like feelings of guilt and low self-assertiveness were also associated with an increased risk of MI.
Patients with MDD (a score of 10 or more on the Beck Depression Inventory [BDI]) had a rate of death due to MI at 1-year follow up that was almost five times higher than patients without depression – a risk ratio that remained after controlling for baseline electrocardiographic evidence of ischemia, left ventricular ejection fraction, and number of diseased coronary arteries.
In all these studies, the relationship between anxiety and poor cardiac outcomes was independent of traditional cardiovascular risk factors and there was evidence of a dose–response effect whereby higher levels of anxiety correlated with poorer cardiac health outcomes. In addition, mental stress has been shown to cause coronary artery vasoconstriction in even normal coronary artery segments for people with and without CAD (118). Similar high rates of postoperative depression and anxiety have been observed in the year following transplantation, with post-traumatic stress disorder being the primary diagnosis (130). HLS included a low-fat, high-fiber vegetarian diet, moderate aerobic exercise, and stress management through Rajyoga meditation.
Although originally developed to diagnose GAD, the GAD-7 is also proven to have good sensitivity and specificity as a screener for panic, social anxiety, and post-traumatic stress disorder (227). Significantly, this correlation did not change after adjustment for body mass index (BMI), premature parental heart attack, cholesterol level, smoking, hyperlipidemia, hypertension, and diabetes mellitus. In the study by Vaccarino, depressive symptoms of 391 patients 50 years old or older who were hospitalized with CHF were measured, and all patients were followed for 6 months with a focus on mortality and functional capacity (activities of daily living [ADL]). At 2-year follow up, subjects with the most adherence to the HLS program had experienced slightly more than 18% ± 12 absolute percentage points diameter stenosis regression and substantial reduction in cardiac events compared to subjects with the least adherence to the study protocol. In this study, mortality at 6 months was two to three times higher in patients with greater depressive symptoms compared to patients with lesser symptoms or patients considered to have normal mood. Patients with moderate depressive symptoms also experienced significant functional declines during follow up.



What to do about ringing in ears after loud music
How to treat tinnitus with drugs
Noise in the ear
What causes clicking in your ears


Comments to “Symptoms of severe depression and anxiety”

  1. 202:
    High mileage and synthetic oil further hearing.
  2. SHCWARZKOPF:
    Adapted to the new reality, and symptoms resolve, usually as treatment while.