Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise tolerance in patients with normal cardiac function can improve with an exercise program. Controversy exists whether this is also true for patients with congestive heart failure (CHF). The limiting symptoms in patients with CHF are shortness of breath and fatigue. Hemodynamic parameters do not correlate well with exercise capacity in patients with CHF. These symptoms may be more related to factors that cause fatigue during exercise than to hemodynamic parameters or even to changes in pulmonary capillary pressure. The factors that cause symptoms include an increased lactate production and metabolic and blood flow abnormalities in the skeletal muscle. Exercise training can improve vasodilation and oxidation capacity, thereby reducing lactate production. Exercise programs may improve exercise capacity in the majority of patients with CHF due to coronary artery disease or idiopathic cardiomyopathy. However, certain patients with ischemia and with anterior infarctions may experience a detrimental effect on their cardiac function. Further studies are needed to better enable recognition of these patients but until this is possible, good clinical judgement must suffice.
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PMID:Cardiac rehabilitation for heart failure patients. 268 76

Congestive heart failure affects over 2.3 million Americans; approximately 400,000 new cases are diagnosed yearly in this country. Congestive heart failure is a complex disorder with a poor long-term prognosis. The major causes of congestive heart failure are ischemia, infarction, and idiopathic cardiomyopathy. Patients often present with dyspnea and a low exercise tolerance. In congestive heart failure there may be an alteration in preload, afterload, and contractility of the heart. Many compensatory mechanisms occur to support the failing heart. Cardiac symptoms slowly develop and eventually systemic symptoms develop. The cornerstones of pharmacologic therapy are cardiac glycosides, diuretics, and angiotensin-converting enzyme inhibitors.
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PMID:Current trends in the primary care management of chronic congestive heart failure. 806 52

Heart transplantation is not yet socially acceptable in the Middle East, and left ventricular assist facilities are not generally available in this region. Therefore, left ventricular volume reduction surgery was attempted in 41 patients with end-stage heart failure (33 males; median age, 36.3 years) in 4 Middle Eastern tertiary referral centers between February 1996 and January 2001. Heart failure was due to idiopathic cardiomyopathy in 21 patients, ischemia in 11, rheumatic valvular disease in 8, and viral myocarditis in 1. Associated procedures were aortic valve replacement in 5 patients, mitral valve repair in 25, mitral valve replacement in 7, tricuspid valve repair in 6, and coronary bypass grafting in 8. Hospital mortality was 31.7%. Five patients were lost to follow-up. The survival rate of hospital survivors at 18 months was 65.2%. Three of the surviving patients did not benefit from the operation. Although our results were somewhat disappointing, this operation remains an option for surgeons working in developing areas of the world. It is hoped that better patient selection and new techniques of left ventricular volume reduction that avoid resection of viable muscle will further improve the outcome of this operation.
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PMID:Left ventricular volume reduction surgery in the middle East. 1287 53

Laminin alpha4 chain is a component of extracellular matrix (ECM) laminin-8 and -9 and serves dual roles as a structure protein and as a signaling molecule. The abundance of laminin alpha4 chain transcripts in the heart suggests an important role of this protein in cardiovascular development and function. In this study, we demonstrate that laminin alpha4 deficient mice gradually develop cardiac hypertrophy with impaired function. We show that depletion of laminin alpha4 chain did not alter the levels of dystrophin-glycoprotein complex (DGC) components or affect cell membrane integrity. No alteration in integrin beta 1D protein was observed in terms of expression level or distribution pattern, indicating that the postnatal development of cardiac hypertrophy and cardiomyopathy in these mice is unlikely associated with the stability of sarcolemmal DGC and integrin complexes. Moreover, cardiomyocytes isolated from Lama4-/- mutant hearts maintained their contractility in vitro. In contrast, elevated levels of hypoxia-inducible factor 1alpha (Hif1alpha) and vascular endothelial growth factor A (Vegfa) transcripts, along with multiple foci of cardiomyocyte degeneration and fibrosis suggested sustained cardiac ischemia. Electron microscopy confirmed malformed blood vessels and wide pericapillary ECM spaces, suggesting the presence of microcirculation abnormalities in Lama4-/- mutant hearts. We thus conclude that mutation in the laminin alpha4 chain leads to abnormal cardiovascular ECM structure that cause insufficient oxygen supply to the heart and the subsequent ischemic cardiac phenotype observed. Our study links the genetic deficiency of an ECM protein to cardiomyopathy and implies a novel pathway of idiopathic cardiomyopathy in human.
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PMID:Cardiomyopathy associated with microcirculation dysfunction in laminin alpha4 chain-deficient mice. 1620 54

Hypertrophic cardiomyopathy (HCM) is classified as a primary cardiomyopathy. HCM is a clinically heterogeneous but relatively common autosomal dominant genetic heart disease that probably is the most frequently occurring cardiomyopathy. HCM is characterized morphologically and defined by a hypertrophied, nondilated left ventriculum (LV) in the absence of another systemic or cardiac disease that is capable of producing the magnitude of wall thickening evident (e.g., systemic hypertension, aortic valve stenosis). Most HCM patients have the propensity to develop dynamic obstruction to LV outflow under resting or physiologically provocable conditions, produced by systolic anterior motion of the mitral valve with ventricular septal contact. The phenotypic features of HCM may develop at any age from infancy to adulthood, and are characterized by a great heterogeneity in the extent, magnitude, and distribution of left ventricular hypertrophy. Hypertrophic obstructive cardiomyopathy (HOCM) often leads to heart failure, severe ischemia, severe symptoms and death. Determination of the exact site of the hypertrophy and of the obstruction of the left ventricular outflow tract, in asymmetric septal hypertrophy, establishes which is the best treatment strategy. In the treatment of HOCM, drug therapy with negatively inotropic drugs, percutaneous transluminal septal myocardial ablation by alcohol-induced septal branch occlusion, surgical myectomy and DDD pacemaker therapy are considered the therapeutical options. We present a case of an obstructive hypertrophic cardiomyopathy in an 84-year-old Italian woman with a left ventricular outflow tract (LVOT) peak gradient with the Valsalva maneuver of 188 mm Hg and with a history of first episode of syncope.
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PMID:Revelation of an obstructive hypertrophic cardiomyopathy in an elderly patient. 1918 3

Diabetic cardiomyopathy is a type of cardiac dysfunction resulting from diabetes, independent of vascular or valvular pathology. It clinically manifests initially as asymptomatic diastolic dysfunction and then progresses to symptomatic heart failure. Two major contributors to the development of diabetic cardiomyopathy, which are unique to diabetes, are hyperglycemia and diabetes-related alterations in myocardial metabolism. Diabetes mellitus is characterized by reduced glucose and lactate metabolism and enhanced fatty acid metabolism, which are the early consequences of the disease. Studies on the effect of intensive glucose control on heart failure events in patients with diabetes have been conducted with neutral results. However, no study on the effect of metabolic modulators on the prevention of heart failure has been reported. Trimetazidine, a 3-ketoacyl coenzyme A thiolase (3-KAT) inhibitor, shifts cardiac energy metabolism from free fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3-KAT, and is used clinically as an effective antianginal agent. Studies have shown that trimetazidine improves heart function in patients with idiopathic cardiomyopathy and in diabetic patients with cardiac ischemia or heart failure. In addition to being effective, trimetazidine has only mild side effects. Therefore, instead of routine administration of trimetazidine for the treatment of diabetic cardiomyopathy, we hypothesize that the early application of trimetazidine may prevent or ameliorate diabetic cardiomyopathy. In addition to life style modifications, ACEI, ARB, and beta-blockers, which have been recommended in the past, trimetazidine should be administered to those patients with impaired glucose tolerance or patients in the early course of diabetes. In this way, we may reduce the prevalence of heart failure and improve the long-term survival of patients with diabetes through early normalization of the myocardial substrate metabolism.
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PMID:Early administration of trimetazidine may prevent or ameliorate diabetic cardiomyopathy. 2093 48

Cardiomyopathies are defined as cardiac diseases of the myocardium with associated cardiac dysfunction. They are cardiac diseases in which heart muscle disease and/or measurable deterioration of cardiac muscle function occurs due to various causes, such as genetic and sporadic mutations of muscle proteins, as well as external factors such as hypertension, ischemia, and inflammation. In 1995, the WHO/International Society and Federation of Cardiology (ISFC) classified primary cardiomyopathy caused by intrinsic factors into five groups according to the dominant pathophysiology: dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restricted cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and unclassified cardiomyopathy. Among these cardiomyopathies, DCM is the most prevalent and the most common reason for cardiac transplantation in adults and children. Many recent findings indicate that genetic and sporadic mutations of a number of muscle proteins, such as myofibrillar, structural, and Ca(2+) regulating proteins, can cause DCM. In such cases, certain mutations often induce DCM with cardiac arrhythmia that is recognized as a potential trigger of sudden cardiac death. Thus, effective prognostic determination and appropriate cardiac care depend on accurate molecular and genetic diagnoses.
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PMID:Dilated cardiomyopathy: a disease of the myocardium. 2330 33