Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular diastolic function is altered in the majority of patients with cardiac diseases, especially those characterized by myocardial ischemia or hypertrophy. In many circumstances, such abnormalities related to impaired relaxation or reduced distensibility may precede evidence of left ventricular systolic dysfunction. Radionuclide angiography may be adapted to study the rapid filling phase of diastole, the duration of the isovolumic relaxation phase, the relative contributions of rapid filling and atrial systole to left ventricular stroke volume, and the relation between regional nonuniformity of left ventricular function and global filling properties. Technical aspects of data acquisition that must be considered for such studies include the effects of cardiac cycle length fluctuations, temporal resolution, temporal smoothing, and normalization parameters. As noninvasive radionuclide methods (and any other analyses using purely noninvasive techniques) do not permit assessment of the left atrial-left ventricular pressure gradient or the simultaneous evaluation of changes in left ventricular pressure and volume during relaxation and filling, complete clinical interpretation of "abnormal" left ventricular filling indexes, or changes in these indexes after interventions, is not possible. Despite the inherent limitations of noninvasive assessment of left ventricular diastolic function, radionuclide evaluation of left ventricular filling may provide clinically useful insights, especially in patients with congestive heart failure symptoms and normal left ventricular systolic function.
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PMID:Radionuclide angiographic evaluation of left ventricular diastolic function. 188 88

Antihypertensive drugs have various effects, both positive and negative, on metabolic and hemodynamic risk factors for coronary artery disease. Cardioprotective effects of angiotensin-converting enzyme (ACE) inhibitors have recently been described. The benefits of ACE inhibition include not only a reduction in blood pressure but also improved insulin responsiveness, prevention of potassium loss, diminished myocardial oxygen demand, suppression of catecholamines, and interaction with bradykinin and prostaglandins. These benefits result in improved perfusion of vital organs, diminished cardiac work, and protection of coronary vessels, evident in improved left ventricular systolic and diastolic function, elevation of the anginal threshold in ischemic heart disease, and decreased morbidity and mortality in congestive heart failure.
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PMID:Cardioprotective potential of angiotensin-converting enzyme inhibitors. 189 45

The nitrovasodilators, nitroglycerin and sodium nitroprusside, cause both arterial and venous smooth muscle dilation by the intracellular release of nitric oxide. Nitric oxide activates guanylate cyclase, resulting in an accumulation of cyclic GMP. The endogenous formation of nitric oxide results in vasodilatory activity similar to the nitrovasodilators. Nitroglycerin is commonly used in the treatment of angina pectoris because of its ability to decrease myocardial oxygen consumption. Most likely, this response occurs as a result of a reduction in preload, which can decrease arterial wall tension and improve coronary blood flow. This pharmacologic effect warrants the use of nitroglycerin in the treatment of myocardial ischemia or infarction, congestive heart failure, and hypertension. Sodium nitroprusside is effective in reducing arterial blood pressure in hypertensive crisis as a result of systemic vasodilation leading to a reduction in preload and afterload. Sodium nitroprusside is not as effective in the treatment of angina pectoris or in diminishing of myocardial ischemia because it does not preferentially improve blood flow to ischemic myocardium over nonischemic myocardium. Inhibition of platelet aggregation has been demonstrated with these drugs, but the clinical applications need further investigation. Nursing interventions for the patient on nitrovasodilator therapy include careful hemodynamic monitoring and drug infusion, along with elimination of physical and emotional stimuli that can aggravate the patient's underlying pathology.
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PMID:Pharmacology of the nitrovasodilators. Antianginal, antihypertensive, and antiplatelet actions. 190 76

Calcium antagonists impede the entry of calcium into myocytes and inhibit myocardial contraction. Calcium antagonists differ in their relative negative inotropic potency and can provoke baroreceptor stimulation that modulates left ventricular (LV) performance. Calcium antagonists are uniformly well tolerated in patients with normal LV function. Use of these agents in patients with suspected LV function impairment has yielded results ranging from hemodynamic improvement to clinical deterioration and increased mortality. Reports of clinical deterioration when calcium antagonists were combined with beta blockers underscore the importance of reflex adrenergic support for the myocardium. Although calcium antagonists are potent vasodilators and produce short-term hemodynamic improvement, they are not useful as primary treatment in patients with congestive heart failure (CHF). They may have a place in the treatment of coexistent problems in patients with LV dysfunction. Short-term use of calcium antagonists for myocardial ischemia or rapid atrial fibrillation is probably safe in the presence of LV dysfunction and overt CHF. Calcium antagonists appear to have a role in the treatment of patients with diastolic dysfunction of diverse etiologies.
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PMID:Calcium antagonists and left ventricular function. 195 Nov 4

Changes in number and/or affinity of cardiac neurotransmitter receptors have been associated with myocardial ischemia and infarction, congestive heart failure, cardiomyopathy, as well as diabetes or thyroid-induced heart muscle disease. These alterations of cardiac receptors have been demonstrated in vitro on membrane homogenates from samples collected mainly during surgery or post mortem. The disadvantage of these in vitro binding techniques is that receptors lose their natural environment and their relationships with the other components of the tissue. In vitro autoradiographic techniques in human tissue offer several advantages over homogenate-binding techniques: an increase in sensitivity and the possibility of anatomic resolution allowing light microscopic mapping of relationships between the distribution of specific cell populations and neurotransmitter receptors. However, the evolution of receptor changes as the disease progresses or as the effect of a drug cannot be analyzed. With the advent of positron emission tomography it is now possible to achieve, non-invasively, quantitative determination of regional biochemical processes in the heart.
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PMID:Cardiac receptors studied by positron emission tomography. 196 75

Despite considerable interest in the use of beta-blocking agents in congestive heart failure (CHF), their clinical application is limited because of their negative inotropic effects. Beta blockers with vasodilating properties may have the advantage of overcoming this, however. Carvedilol, a beta-blocking agent with vasodilating properties, was evaluated in 17 patients with chronic CHF secondary to ischemic heart disease with a resting left ventricular ejection fraction less than or equal to 45%, who were being maintained on diuretics. Exercise testing, radionuclide ventriculography, and right-sided cardiac catheterization were performed and intraarterial blood pressure measured before and after 8 weeks of carvedilol therapy in a dosage of 12.5 to 50.0 mg twice a day. Twelve patients completed the study and 5 withdrew. Symptomatic and hemodynamic improvement was demonstrated in 11 of the 12 patients. Heart rate and intraarterial blood pressure were both reduced by chronic therapy. Mean +/- standard deviation exercise time improved from 4.3 +/- 1.6 to 7.1 +/- 2.7 minutes (p less than 0.0001), as did resting left ventricular ejection fraction, from 27 +/- 9 to 31 +/- 11% (p less than 0.02). Pulmonary arterial wedge pressure fell from 19 +/- 7 mm Hg to 12 +/- 5 mm Hg (p less than 0.001) and total systemic vascular resistance from 1,752 +/- 403 to 1,497 +/- 310 dynes/s/cm-5/m2 (p less than 0.02). Stroke volume index improved also, from 31 +/- 6 ml to 40 +/- 6 ml (p less than 0.0005). These hemodynamic changes were mediated partly by vasodilation, diminished myocardial oxygen demand and reduction of sympathetic overactivity in the failing heart. These data suggest that carvedilol may have beneficial effects in patients with chronic CHF secondary to coronary artery disease.
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PMID:Value of carvedilol in congestive heart failure secondary to coronary artery disease. 197

Noninvasive risk assessment in survivors of AMI can effectively subdivide patients into groups with differing risk profiles after hospital discharge, but some patients at risk for late death or recurrent AMI may be incorrectly identified; data from cardiac catheterization and angiography provide complementary and generally more powerful prognostic information. Many patients may derive particular benefit from early cardiac catheterization and angiography, including: (1) patients with AMI complicated by recurrent myocardial ischemia, congestive heart failure, and/or complex ventricular arrhythmias; (2) patients with abnormal or inconclusive results of noninvasive testing or those patients unable to perform an exercise test; (3) patients with abnormal left ventricular global systolic function and those with increased left ventricular end-systolic volume; (4) "young" patients (younger than 50 years of age?); (5) older patients (older than 65 to 70 years of age?); (6) patients with non-Q wave AMI; and (7) patients who are receiving thrombolytic therapy. Performance of early cardiac catheterization and angiography in virtually all survivors of AMI, with selective use of appropriate noninvasive tests, may provide a more efficacious means of risk assessment after AMI; if all tests are performed judiciously, the cost of such an approach need not be excessive. A combination of invasive and selected noninvasive tests probably provides optimal information. The risks to the routine performance of diagnostic cardiac catheterization and angiography in all survivors of AMI are: (1) adequate care and attention may not be paid to proper performance of the procedure(s) and to detailed and proper analyses of the data; (2) the need for additional noninvasive testing in selected patients may be ignored; and most importantly, (3) premature or unnecessary revascularization procedures may be performed subsequently. For optimal patient care, the clinician must obtain all necessary data, avoid unnecessary and repetitive tests, know the accuracy of individual tests at his or her own facility, interpret all data in proper context, and then counsel patients objectively about available management strategies. With this approach, all patients who might appropriately benefit from coronary artery revascularization will be correctly identified, and patients who are truly at very low risk (minimal residual coronary artery disease and preserved left ventricular function particularly if associated with a patent infarct-related artery) may be similarly identified and managed appropriately with elimination of unnecessary additional testing and pharmacologic therapy. Finally, whatever approach to risk stratification one chooses for an individual patient, the importance of and the need to correct and/or ameliorate risk factors for coronary artery disease must be recognized and undertaken.
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PMID:Risk stratification in survivors of acute myocardial infarction: routine cardiac catheterization and angiography is a reasonable approach in most patients. 199 Jul 80

This study reviewed 372 male patients with congestive heart failure. Two hundred and eighty-three (77%) had congestive heart failure due to systolic dysfunction as demonstrated by radionuclide angiography. Eighty-seven (23%) with congestive heart failure were identified who had normal ejection fractions. All patients met the Framingham criteria for congestive heart failure. These 87 individuals had unrecognized diastolic heart failure. It is important to distinguish between systolic and diastolic heart failure because the pathophysiology, treatment, and prognosis differ significantly. The most frequent cause of diastolic heart failure in this study was hypertension. Diastolic dysfunction should be considered in patients with acute heart failure and severe uncontrolled hypertension, or in patients with ischemic heart disease who develop acute pulmonary edema. Patients who do not respond or deteriorate when treated for heart failure using conventional therapy may also have diastolic dysfunction. These patients warrant special recognition and tailored management.
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PMID:Left ventricular diastolic dysfunction in patients with congestive heart failure. 199 65

Therapeutic uses of calcium antagonists have expanded to include not only ischemic heart disease but arrhythmias, systemic hypertension, congestive heart failure and various pulmonary and gastrointestinal diseases. Many patients receiving calcium antagonists concomitantly receive digoxin. Although the potential interactions between these agents have frequently been investigated, literature reports are confusing and inconsistent. The pharmacokinetics and mechanisms of interaction are summarized in order to help clinicians to evaluate the potential calcium antagonist digoxin interaction. From the investigations to date, changing the digoxin dosage prior to initiating calcium antagonist therapy is, however, not justifiable. The best approach would be to monitor pharmacodynamic values, SDC, and the patient's clinical status.
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PMID:[Interaction between calcium antagonists and digoxin]. 202 27

Cardiac conduction defects have not been previously described in association with hyponatremia, although in patients with congestive heart failure the frequency of ventricular premature beats was found to correlate to the severity of hyponatremia. We describe three patients with second-degree or complete atrioventricular (AV) block which occurred during or shortly after an episode of severe hyponatremia. The first had thiazide-induced hyponatremia while on amiodarone. In the second, definite etiology for hyponatremia which was associated with longstanding polydipsia could not be established. The third had ischemic heart disease and intermittent conversion of his first-degree to second-degree AV block while hyponatremic after diuretics use. Although it is usually difficult to single out hyponatremia as the cause of conduction defects which usually occur in the presence of cardiac disease, potent medications or other electrolyte abnormalities, we suggest that hyponatremia may play a role in the pathogenesis of conduction defects in the diseased heart.
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PMID:Cardiac conduction defects associated with hyponatremia. 204 46


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