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07.03.2015

Drugs and heart disease, continuous ringing noise in ear - PDF Review

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Heart failure afflicts 1-2 per cent of the general population and 6-10 per cent of the elderly (<65 years) population in developed nations. The current treatments of heart failure address normalisation of its symptoms by using pharmacological agents to improve contractile performance.
In order to understand the disease progression of heart failure, it is necessary to understand the changes to heart contractile function at the cellular level. The physiological symptoms of cardiac hypertrophy and heart failure are accompanied in part by renewed expression of the fetal cardiac genes i.e. Another important class of transcription factor involved in the advent of heart failure are proteins that regulate the histone proteins. The export of class II HDAC requires activation of calmodulin kinase II and local calcium release from perinuclear IP3. Protein kinase D also regulates HDAC through a related pathway as follows: Activation of phospholipase C, typically in response to agonist cleaves phosphatidyl inositol into Diacylglycerol (DAG) and IP3. In summary, recent experiments have given insight into the complex signalling pathways associated with cardiac hypertrophy and heart failure. Oct 14, 2012 two different studies conclude that the use of statin drugs may increase the calcification of coronary artery, which leads to lethal heart disease.
Cholesterol-lowering statins are heavily promoted for heart patients but research is calling into question their use as a preventive medicine. If used properly, prescribed medications can improve your loved ones health, but you should also be aware of the medications potential side effects. Heart disease reference guide covers symptoms, causes, treatments and prevention of heart disease. There is a direct connection between drug abuse and alcoholism and irregular heartbeat, collapsed veins, bacterial infections, cardiovascular distress, heart attack. Combined alpha and beta-blockers are used as an iv drip for those patients experiencing a hypertensive crisis.
The incidence of diabetes is rising rapidly and patients with diabetes have a significantly increased risk of developing cardiovascular disease.
The approach to diabetes management in patients with stable, established coronary heart disease is similar to those with no cardiac history. Type 1 diabetes requires exogenous insulin treatment and metformin is used in some cases as an insulin-sensitising agent. For patients with type 2 diabetes, treatment requires more consideration due to the increasing choice of medications available and the recent conflicting evidence regarding intensity of diabetes control. The UK Prospective Diabetes Study (UKPDS) and its 10-year follow-up showed that early intensive glycaemic control, this time in type 2 diabetes, would also lead to later cardiovascular benefit or ‘legacy effect’ despite relaxation of HbA1c target outside of the study.6 Patients with coronary heart disease were excluded from the UKPDS at baseline, but on follow-up MI was the most common cause of death. The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial set out to assess whether intensive glycaemic control in patients with established type 2 diabetes, cardiovascular disease, or high cardiovascular risk would provide cardiovascular benefit.
Management of type 2 diabetes must be holistic and includes education, lifestyle intervention and medication. Sulphonylureas, which stimulate pancreatic insulin secretion, and insulin are associated with hypoglycaemia and weight gain, both are side effects that can increase cardiac stress in diabetes.4,11 In UKPDS, the sulphonylurea gliclazide was found to have a non-significant risk reduction for MI. In 2010, rosiglitazone lost its European recommendation and the FDA significantly restricted its use in the USA. The FDA mandated a trial comparing rosiglitazone and pioglitazone on cardiovascular outcomes.
The DPP-4 inhibitors and GLP-1 receptor agonists are both classes of drug working on the incretin system, which amplifies insulin secretion in response to oral carbohydrate intake.18,19 They are attractive treatment options for type 2 diabetes given that they have low risk of hypoglycaemia, similar effect on HbA1c and do not cause weight gain.
DPP-4 inhibitors, such as sitagliptin, vildagliptin and saxagliptin, were found to non-significantly reduce cardiovascular events in a recent meta-analysis.20 Several large randomised-controlled trials of cardiovascular safety are ongoing, including one designed to show non-inferiority of sitagliptin versus placebo and one to show superiority of saxagliptin over placebo. GLP-1 receptor agonists, such as exenatide and liraglutide, require subcutaneous injection and commonly cause weight loss. The Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study was a trial of intensive insulin following acute MI in patients with diabetes, which found a prognostic benefit of acute insulin-glucose infusion followed by at least three months of subcutaneous insulin.23 DIGAMI-2 was set up to establish whether the benefit came from the acute intravenous insulin or the three months of intensive subcutaneous insulin by having three trial groups. Recent National Institute for Health and Clinical Excellence (NICE) guidance has been published on the management of hyperglycaemia in acute coronary syndrome.25 Hyperglycaemia is common in patients who do not have a diagnosis of diabetes and is a risk factor for future development of diabetes.
Following the first 48 hours of care, the choice of antidiabetic drugs will depend on the clinical picture and pre-existing diabetes control. People with diabetes have a higher incidence of chronic heart failure and are more likely to develop heart failure at a younger age.28 Poor glycaemic control, blood pressure and obesity are modifiable factors that contribute to risk of cardiovascular disease. Concerns about the use of metformin in heart failure exist due to the potential to develop lactic acidosis in hypoperfused states, and it is common practice to discontinue metformin during episodes of acute heart failure. Despite its associated weight gain, there is no direct evidence of insulin worsening heart failure in the majority of patients. Cardiovascular disease is arguably the most important complication of diabetes and is an important outcome in clinical trials as new drugs for diabetes must now prove their cardiovascular safety prior to approval. Your doctor may prescribe a variety of heart medications you can take to treat or prevent heart disease. Do not take any over-the-counter drugs or herbal therapies unless you ask your doctor first. Before having surgery with a general anesthetic, including dental surgery, tell the doctor or dentist in charge what heart drugs you are taking. Making some simple changes in what you eat, how often you exercise, how much you weigh, and how you manage stress can help to put the brakes on heart disease.


Dean Ornish, MD, founder and president of the Preventive Medicine Research Institute, has written six best-selling books, including Dr. Diet may be the biggest thing you’d change to try to reverse heart disease as much as possible. Ornish’s book, The Spectrum, puts foods in five groups, ranging from healthiest to least healthy. Ornish agrees that if you’re just trying to slow heart disease, you might have more freedom with your diet. For example, drugs such as digitalis can improve beat-to-beat force generation, drugs such as Angiotensin Converting Enzyme (ACE) inhibitors and β-blockers modulate neurohumeral signalling to enhance contractile performance, and drugs such as calcium channel blockers normalise cardiac calcium handling. Heart failure is characterised by changes in the expression of the proteins governing ionic currents and calcium handling. Get an overview on drugs such as beta blockers, diuretics and ace inhibitors and what they do. The cardiovascular risk associated with diabetes means that use of statins and angiotensin-converting enzyme (ACE) inhibitors is standard above the age of 40 years (table 1).
Insulin can be delivered as a twice-daily fixed mixture or with multiple-daily injections (MDI) of basal and prandial insulin or even as a continuous subcutaneous insulin infusion (CSII).
The intensive group had a 42% reduction in any cardiovascular event and a 57% reduction in nonfatal myocardial infarction (MI), stroke or cardiovascular death.5 These benefits were retained despite returning to standard care after DCCT and have been referred to as ‘metabolic memory’ or ‘legacy effect’.
There are now several newer antidiabetic drugs available, in addition to the well-established metformin, sulphonylureas and insulin.
Insulin is reserved for third-line treatment in type 2 diabetes and when introduced should be a once-daily long-acting dose. The Thiazolidinedione Intervention with Vitamin D Evaluation (TIDE) trial had just started recruiting patients when it was stopped prematurely by the FDA: 16,000 patients were to be randomised using a 3 x 2 design (the other part of the study comparing Vitamin D and placebo). Patients with type 1 diabetes and poor control may have increased interest in intensifying their insulin, perhaps from twice-daily mixed insulin to multiple-daily injections with the option of carbohydrate counting. Lifestyle advice should be given and warning about future risk of diabetes, which should be screened for annually.
For those on metformin there is concern regarding the potential risk of lactic acidosis when given at times of tissue hypoxia, but there is no conclusive evidence to suggest metformin should not be used following MI.26 If metformin is the sole agent, it is also important to consider the glycaemic impact of removal peri-angiography when the contrast load in combination with metformin may potentially lead to renal impairment and lactic acidosis.
It may be opportune to consider glycaemic control when managing patients with heart failure, many of whom will have co-existent renal failure.
The effect of intensive treatment of diabetes on the development and progression of long-term complications of insulin-dependent diabetes mellitus. Epidemiological relationships between A1C and all-cause mortality during a median 3.4 year follow-up of glycaemic treatment in the ACCORD trial.
Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. The effect of pioglitazone on recurrent myocardial infarction in 2,445 patients with type 2 diabetes and previous myocardial infarction: results from the PROactive (PROactive 05) study.
Pioglitazone use and heart failure in patients with type 2 diabetes and pre-existing cardiovascular disease: data from the PROactive (PROactive 08) study. Efficacy and safety of the human glucagon-like peptide-1 analog liraglutide in combination with metformin and thiazolidinedione in patients with type 2 diabetes (LEAD-4 Met+TZD). Intensive metabolic control by means of insulin in patients with acute myocardial infarction (DIGAMI 2): effects on mortality and morbidity. Impact of type of pre-admission sulphonylureas on mortality and cardiovascular outcomes in diabetic patients with acute myocardial infarction. Benefits and harms of antidiabetic agents in patients with diabetes and heart failure: systematic review. The risk of heart failure in patients with type 2 diabetes treated with oral agent monotherapy.
Congestive heart failure and cardiovascular death in patients with prediabetes and type 2 diabetes given thiazolidinediones: a meta-analysis of randomized clinical trials. Insulin resistance and glycaemic abnormalities are associated with deterioration of left ventricular diastolic function: a cross-sectional study. These drugs may help lower your blood pressure, reduce the level of cholesterol in your blood, or help the body get rid of excess fluids that put a strain on the heart’s ability to pump blood.
Whatever the treatment protocol prescribed to you, it is a good idea to keep the following guidelines in mind when you’re taking heart disease drugs.
The prescription label tells how much to take at each dose, but your doctor may change the dosage periodically, depending on your response to the drug. Some drugs, such as antacids, salt substitutes, antihistamines (including Benadryl and Dimetapp), and nonsteroidal anti-inflammatory agents (NSAIDs, such as Advil, Motrin, and Indocin), can worsen heart failure symptoms.
On longer trips, take an extra week’s supply of medications and copies of your prescriptions, in case you need to get a refill. So are sticking to a healthy weight, taking all your medications, keeping up with your doctor visits, and not smoking or being around secondhand smoke.
New experimental findings suggest possible future therapies that arrest the development of heart failure.
There is a growing incidence of reported heart failure in other parts of the world including Asia, Africa and the Middle East. Furthermore, it has been shown that exercise helps to normalise cardiac function by reversing some of the systemic changes seen during heart failure.


Curcumin blocks phenylephrine- and pressure overload-induced cardiac hypertrophy in primary cultured rat cardiac myocytes through inhibition of P-300 HAT activity. Due to the complexities of the signalling pathways, further studies are likely to additional drug targets and lead compounds.
Previous positions include Assistant Professor at University of Texas at Dallas, Research Associate at Johns Hopkins University, and post-doctoral researcher at University of California, Davis. Multimedia health information for patients, caregivers and providers supplied by harvard medical school. Drugs that help millions of people cope with acid reflux may also cause cardiovascular disease, report scientists from houston methodist hospital and two other. Mar 15, 2015 coronary heart disease (chd) is a narrowing of the small blood vessels that supply blood and oxygen to the heart. If you think you have heart disease or are worried about your heart disease risk because of your family history, see your family doctor.
Patients with stable coronary disease can be treated with metformin, sulphonylureas or pioglitazone.
Intensive glycaemic control is desirable to limit microvascular complications,1 but, in those with established diabetes, aggressive blood-glucose lowering may be detrimental.2 The oral antidiabetic drug, rosiglitazone, has recently been removed from the European market due to its perceived lack of cardiovascular safety.
The newer agents include oral dipeptidylpeptidase-4 (DPP-4) inhibitors and injected glucagon-like peptide-1 (GLP-1) agonists.
The method for this glycaemic control is patient dependent, but a dose-adjusted insulin infusion should be considered with regular blood glucose monitoring and avoidance of hypoglycaemia. Recent large trials assessing the impact of glycaemic control on cardiovascular risk highlight the importance of individualised care and addressing other modifiable cardiovascular risk factors in order to gain long-term benefit. If you have trouble getting to the pharmacy, have financial concerns, or have other problems that make it difficult to get your heart drugs, let the doctor know. You’ll fill your plate with fruits and vegetables, whole grains, legumes, soy products, nonfat dairy, and egg whites, and avoid fats, refined sugar, and processed carbs. Pathological cardiac hypertrophy exhibits increased ventricular-wall tension and cardiac contractile dysfunction, and is a major predictor of heart failure.
In spite of these therapies, there currently exist no approved drugs that can reverse or prevent the development of heart failure. This reduction in DAG concentration reduces class II HDAC export from the nucleus through protein kinase C and D. Following an acute coronary syndrome, intensive insulin therapy with multi-dose insulin has been shown to reduce mortality, and longerterm treatment with pioglitazone may reduce recurrent events.
In 2008, the Food and Drug Administration (FDA) issued recommendations that all new drugs for diabetes should provide data regarding cardiovascular safety, in addition to glycaemic control, prior to approval. Norepinephrine (NE), Phenylephrine (PE), or Isoproterenol (ISO), and pressure-overload hypertrophy induced by banding of the thoracic aorta. The elevation of intracellular calcium is a common regulatory factor in both NFAT import into the nucleus and class II HDAC export from the nucleus.
Additionally, DAG kinase has been shown to suppress cardiac hypertrophy and loss of left ventricular function in mice.
There is little trial information for glycaemia control in patients with chronic heart failure, and metformin and insulin are both frequently used. It is important to consider both the impact on glycaemic control and cardiovascular risk when prescribing drugs for diabetes. Inhibitors of class I HDAC such as tricostatin A, sodium butyrate, and HC-toxin block cardiac hypertrophy and improve contractility in failing hearts.
It blocks endothelin-1 induced growth and activation of fetal gene programs caused through the PKC pathway.
Aug 29, 2014 a new study reports one of the biggest potential advances against heart failure in more than a decade a first-of-a-kind, experimental drug that lowered. Dipeptidylpeptidase-4 (DPP-4) inhibitors are new oral antidiabetic drugs, which are weight neutral, and the injected glucagon-like peptide-1 (GLP-1) receptor agonists reduce weight. In the heart, the cytosolic calcium concentration is elevated periodically as calcium is elevated to cause contraction of the myocyte. Expert advice on heart medication, including the dangers of skipping doses, aspirin for heart health, tips on statins and blood pressure drugs, and more. If a clot can becomes lodged in a heart vessel, it can partially or completely prevent blood from flowing anywhere past the clot.
A number of investigators have suggested that the periodic release of contractile calcium can trigger activation of the transcription factors that lead to hypertrophy and heart failure. In fact, knockout of class II HDACS produced spontaneous hypertrophy in mice and antiviral overexpression of active mutants of class II HDAC prevented agonist-induced hypertrophy in cultured myocytes. For example, the rapid pacing (tachycardia) of the canine ventricle by an implanted electrode (about four beats a second or 4 Hz) for prolonged periods has been used to induce hypertrophy and heart failure.
Furthermore, other work has shown that in neonatal rat ventricular myocytes, exposure to angiotensin II caused an increase in the rate of contractile cytosolic calcium transients and an increase in the amount of NFAT translocated to the nucleus.
Furthermore, NFAT transclocation to the nucleus can be blocked by immunosuppresants such a cyclosporin A and FK506.



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