Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of primary hyperparathyroidism (PHPT) in heart disease is still somewhat uncertain in many respects. Patients with PHPT seem to have an increase in mortality and this seems mainly due to an overrepresentation of cardiovascular death. PHPT is reported to be associated with hypertension, disturbances in the renin-angiotensin-aldosterone system, cardiac arrhythmias as well as structural and functional alterations in the vascular wall. There is an increased prevalence of cardiac structural abnormalities such as LVH and functional properties of the heart may be affected by the hyperparathyroid condition as well. We report the case of a 65-year-old woman with no cardiac risk factors apart from her age and type 2 diabetes who presented in cardiogenic shock. Extensive evaluation for the aetiology of the cardiomyopathy revealed solely a diagnosis of primary hyperparathyroidism. Cardiac manifestations of primary hyperparathyroidism have been reported before but to our knowledge this is the first description of severe left ventricular function secondary to PHPT. We believe that this atypical presentation of primary hyperparathyroidism causing left ventricular cardiomyopathy warrants further attention, and that a diagnosis of primary hyperparathyroidism should always be considered in patients with systolic as well as diastolic left ventricular dysfunction, and no other obvious cause.
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PMID:Primary hyperparathyroidism and the cardiovascular system. 1691 43

Nonsteroidal antiinflammatory drugs (NSAIDs) have potentially important renal adverse effects. With regard to renal adverse effects there is no indication of significant differences between conventional NSAIDs and selective COX-2 inhibitors. Their nephrotoxicity has been well documented. Many of the renal abnormalities that are encountered as a result of NSAIDs use can be attributed to the inhibition of prostaglandins synthesis. The release of prostaglandins is particulary importent in high-risk patients, including patients with severe heart disease, liver disease, preexisting renal disease, elderly and patients with volume depletion. The common complication of NSAID use is retention of sodium and edema formation due to increased reabsorption of sodium and water in the loop of Henle and hyperkalemie due to diminished renin secretion. Nonsteroidal antiiflammatory drugs can induce two different forms of acute renal failure. Decreased prostaglandin synthesis can lead to reversible renal ischemia and hemodynamically-mediated acute renal failure. Second form of acute renal failure is acute interstitial nephritis. This type of interstitial nephritis is often accompanied by nephrotic syndrome due to minimal change disease. Nephrotic syndrome after NSAIDs treatments may be also associated with membranous nephropathy. Another complication of NSAIDs treatment is modest rise of systemic blood pressure in some hypertensive patients due to increase in renal and systemic vascular resistence. In patients consuming excessive amount of NSAIDs over a prolonged period of years papillary necrosis can occur. Exposure to large quantities of NSAIDs can probably induce in some patients chronic renal insufficiency.
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PMID:[Nonsteroidal antiinflammatory drugs and the kidney]. 1696 9

Heart disease and depression are highly co-morbid. Clinical and experimental research over the past 70 years has led to several neurohumoral hypotheses of causative factors present under the conditions of either heart failure or of psychological depression. Some of these hypothesized factors are common to both disorders and are therefore attractive candidates to account for the high incidence of co-occurrence of depression and heart disease. One experimental approach to study the co-morbidity of heart failure and depression has been to study the behavioral, biochemical and physiological changes in a chronic mild stress model of depression and in heart failure induced by experimental myocardial infarction. Our studies have led us to focus on the pro-inflammatory cytokines, in particular tumor necrosis factor (TNF)-alpha, and the renin-angiotensin-aldosterone system. Both of these families of humoral factors are elevated in human heart failure and in depression and the two experimental models we have studied. The demonstrated validity of each of these models will be of great value in elucidating the nature of the actions and interactions of these humoral agents as they contribute to the co-morbid conditions of heart failure and depression.
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PMID:Sadness and broken hearts: neurohumoral mechanisms and co-morbidity of ischemic heart disease and psychological depression. 1724 36

The renin-angiotensin system is primarily responsible for regulating vascular tone. Drugs that inhibit this pathway, angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists, are widely used to treat hypertension and a variety of cardiomyopathies. Recent studies have shown that, in addition to reducing blood pressure, these drugs also modulate inflammation, adhesion molecule expression, and fibrosis. To assess the therapeutic potential of these inhibitory agents for the treatment of inflammatory heart disease, the drugs have been tested in experimental models of infectious and autoimmune myocarditis. This review summarizes the results of studies examining the efficacy of angiotensin converting enzyme inhibitors and angiotensin receptor antagonists for the treatment of mouse models of virus-induced and parasite-induced myocarditis, as well as autoimmune cardiomyopathy. The collective results strongly support the use of renin-angiotensin modulation for the treatment of myocarditis. Importantly, this therapeutic approach seems to downregulate autoimmunity without causing immune suppression which may enhance the survival of the disease-initiating infectious agent.
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PMID:Treatment of experimental myocarditis via modulation of the renin-angiotensin system. 1750 15

Obesity is becoming a worldwide phenomenon. Myocardial changes associated with the obese state are increasingly recognized, independent of hypertension, obstructive sleep apnea and coronary artery disease. The existence of a cardiomyopathy of obesity is supported by a range of evidence: epidemiologic study findings, which have shown an association between obesity and heart failure; clinical studies that have confirmed the association of adiposity with left ventricular dysfunction, independent of hypertension, coronary artery disease and other heart disease; and experimental evidence of structural and functional changes in the myocardium in response to increased adiposity. The most important mechanisms in the development of obesity cardiomyopathy are metabolic disturbances (insulin resistance, increased free fatty acid levels, and also increased levels of adipokines), activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, myocardial remodeling, and small-vessel disease (both microangiopathy and endothelial dysfunction). In the first part of this two-part Review, we seek to evaluate the emerging evidence for the existence of a cardiomyopathy of obesity and clarify the responsible mechanisms.
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PMID:Obesity cardiomyopathy: pathogenesis and pathophysiology. 1765 16

Heart disease and stroke are the most life-threatening consequences of diabetes mellitus, with mortality rates up to two to four times higher for persons with diabetes vs. those without and accounting for up to 65% of deaths. The cardiometabolic syndrome is a potent indicator of future risk of type 2 diabetes and concomitant increased potential for cardiovascular morbidity and mortality. Pharmacologic treatment is usually necessary to improve blood pressure and lipids, thereby decreasing the risk of cardiovascular disease. The reduction of cardiovascular and renal risk with type 2 diabetes and elevated blood pressure are compelling indications for thiazide diuretics, blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and calcium channel blockers. Nevertheless, most patients with type 2 diabetes and elevated blood pressure will require two or more agents to lower blood pressure to the recommended goal of <130/80 mm Hg, and combination therapy may be beneficial. In patients with the cardiometabolic syndrome without type 2 diabetes, the present goal is to maintain BP <140/90 mm Hg, although recent data suggest potential decrease in the progression of prehypertension to hypertension with antihypertensive medication. Furthermore, blockers of the renin-angiotensin system may actually prevent newonset diabetes. It is reasonable for patients with type 2 diabetes and cardiovascular disease to achieve an optional low-density lipoprotein cholesterol (LDL-C) goal <70 mg/dL, and statin therapy should be considered regardless of baseline LDL-C level. In patients with the cardiometabolic syndrome without type 2 diabetes and calculated moderately high-risk status (two or more risk factors; 10-year risk, 10%-20%), the present goal for LDL-C is <130 mg/dL, with perhaps a therapeutic option of <100 mg/dL, and in patients with the cardiometabolic syndrome at lower risk, the LDL-C goal remains <160 mg/dL. Multifactorial management must be utilized to prevent progression of cardiovascular risk with the cardiometabolic syndrome and the ravages of cardiovascular disease in persons with type 2 diabetes, including antiplatelet therapy with aspirin.
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PMID:Management of cardiovascular risk in patients with type 2 diabetes mellitus as a component of the cardiometabolic syndrome. 1767 32

In a large number of patients with hypertension, > or =2 antihypertensive agents are required to achieve blood pressure (BP) goals. There is good rationale for initial combination therapy based on clinical trials demonstrating that achievement of BP goals within a reasonably short period of time results in fewer cardiovascular events. One approach to attaining BP goals and improving medication adherence is fixed-dose combination therapy, the use of which dates back to the 1960s. Given some of the advantages of renin-angiotensin-aldosterone system (RAAS) blockers in patients with heart disease, kidney disease, and diabetes, many combinations include either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. In most studies, however, thiazide diuretics were necessary to achieve goal BP. Calcium channel blockers have also been used in combination with angiotensin-converting enzyme inhibitors to lower BP. Studies are now under way to determine the relative benefits of an RAAS blocker/diuretic compared with an RAAS blocker/calcium channel blocker as initial therapy.
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PMID:Combination therapy with Renin-Angiotensin-aldosterone receptor blockers for hypertension: how far have we come? 1825 79

Hypertension is one of the major health care problems worldwide since it markedly increases the risk for development of heart disease, stroke, generalized vascular disease, and renal failure. The renin-angiotensin system (RAS) with its major end-product angiotensin II (Ang II) plays a fundamental role in blood pressure regulation through direct and indirect mechanisms. Pharmacologically, we can inhibit the RAS using angiotensin-converting enzyme inhibitors and AT1 receptor blocker. Inhibiting renin directly with a clinically useful drug eluded pharmacologists until recently. However, the once-daily, orally effective, small-molecule, direct renin inhibitor aliskiren has recently changed this state of affairs. Aliskiren, with its 40-h half-life and ideal pharmacokinetics, can now address angiotensin production directly at its rate-limiting step. A novel transgenic rat model outfitted with the human renin and angiotensinogen genes allowed the testing of aliskiren in an animal model. Preclinical data demonstrated that aliskiren prolonged survival, decreased cardiac hypertrophy and the inducibility of arrhythmias, proteinuria, and attenuated inflammation. All these features might result in improved target-organ damage. Studies in humans attest to an effective blood pressure-lowering action, a largely side effect-free profile, and the option of several combination therapies. Aliskiren is the first of a novel antihypertensive drug class. The preclinical data is very promising. Nevertheless, for the evaluation of its potency in humans, we have to wait for more clinical data.
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PMID:Aliskiren--mode of action and preclinical data. 1844 51

Inhibition of renin-angiotensin system (RAS) activity using angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (ARBs) is beneficial in patient populations with left ventricular dysfunction or systolic heart failure (HF) and other forms of heart disease. In high-risk patients with coronary heart disease (CHD), treatment with these agents reduces the mortality rate and improves secondary outcomes. Individuals with stable CHD who are at lower risk benefit less from treatment. RAS inhibition also provides some clinical benefit to patients with diastolic HF and preserved left ventricular function. Left ventricular hypertrophy (LVH) is a strong predictor of cardiovascular events and all-cause mortality in patients with hypertension. Treatment with an ARB reduces the risk for adverse cardiovascular outcomes in patients with hypertension and LVH. The benefits correlate with regression of LVH, and the effect is independent of the degree of blood pressure lowering. Finally, studies indicate that a history of hypertension in patients who have not had a myocardial infarction (MI) increases the risk for HF after MI; the risk is decreased in patients with hypertension who receive treatment with a RAS inhibitor.
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PMID:Management of hypertension in patients with cardiac disease: use of renin-angiotensin blocking agents. 1863 17

Nephrologists should promote the detection of CKD in heart disease patients. The evaluation should include estimation of GFR and detection of microalbuminuria in a recently voided urine sample by the albumin:creatinine ratio. Any patient with stage 3 or 4 CKD and rapid deterioration of GFR should be evaluated by the nephrologist. - Patients with CKD have a high risk of cardiovascular (CV) complications and heart disease patients have a high incidence of CKD and progression is also more rapid (Strength of Recommendation B). The most likely pathophysiological hypothesis is endothelial damage. - The CV risk profile should be established in each patient followed by adequate compliance with control goals for common CV risk factors: smoking, obesity, sedentarism, hypertension, dyslipidemia. Early treatment of anemia and bone mineral disease as CV risk factors requires special mention (Strength of Recommendation B). - Management of these patients will be based on individualization of treatment, close systematic follow-up, and integration between care levels: Specialized care (nephrologists and cardiologists) and primary care. - The cardiorenal syndrome (CRS) is a condition in which both organs are simultaneously affected and their deleterious effects are reinforced in a feedback cycle, with accelerated progression of renal and myocardial damage. Because of its prognostic value, treatment of HF takes precedence over CKD. Most studies on cardiovascular risk and on HF exclude patients with stage 4-5 CKD. We thus do not have sufficient strong evidence and recommendations are based on the extrapolation of data from studies with normal GFR or milder grades of CKD, and on the empirical use of certain treatments. - ARBs and ACEIs are the mainstays of treatment of HF with systolic and diastolic dysfunction, and have been shown to reduce mortality in studies in the general population (Strength of Recommendation A). The may also slow progression of CKD, especially in diabetics. Dual renin-angiotensin blockade with the combined use of lower doses of both drugs has shown promising results for control of CKD progression, but there are no data to recommend its use for control of HF in advanced stages of CKD (stage 4-5) (Strength of Recommendation C). - In these stages of CKD, only loop diuretics have sufficient potency. The therapeutic dose range should be achieved. Lowdose thiazides achieve diuretic synergy. The use of spironolactone and eplerenone has shown benefits in patients with AMI and HF with an ejection fraction < 40% without advanced CKD. They should always be used with strict control of GFR and K+. No benefit has been shown for the use of <<dopamine in diuretic doses>> (may even be harmful) or continuous infusion of furosemide (Strength of Recommendation B). The use of beta-blockers should be increased in these patients. - Treatment-refractory heart failure in the context of stage 3 CKD could be amenable to ultrafiltration techniques. Continuous ambulatory PD could be an alternative treatment to maintain hemodynamic equilibrium while also allowing pharmacological treatments to be prescribed that would not be feasible without dialysis and could even improve myocardial and kidney function (Strength of Recommendation C).
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PMID:[Cardiorenal syndrome]. 1901 35


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