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)

We tested the hypothesis that transmural differences in coronary microvascular pressures may be greater in the setting of hypertension and left ventricular hypertrophy. Epicardial and endocardial microvascular pressures were measured in isolated lidocaine-arrested hearts during adenosine vasodilation. In both normotensive (n = 19) and hypertensive (one clip, one kidney, n = 10) dogs, microvascular pressures in endocardial arterioles at 60, 70, 80, 90, and 100 mm Hg of left main coronary perfusion pressures were lower than in epicardial arterioles (p less than 0.05 at all perfusion pressures). The pressures in epicardial arterioles as a percentage of the left main coronary perfusion pressure were similar in normotensive versus hypertensive hearts at all perfusion pressures. In contrast, the pressures in endocardium at 90 and 100 mm Hg of perfusion pressure were significantly (p less than 0.05) lower in dogs with hypertension and hypertrophy than in the controls (41 +/- 4 versus 50 +/- 2 and 40 +/- 4 versus 50 +/- 3 mm Hg at 90 and 100 mm Hg of perfusion pressure, respectively). Thus, there is a greater transmural resistance to microvascular perfusion in hearts with myocardial hypertrophy secondary to hypertension. This is likely due to differences in the vascular anatomy, secondary to hypertension and hypertrophy, and may contribute to vulnerabilities in subendocardial ischemia encountered in this condition.
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PMID:Effect of hypertension and hypertrophy on coronary microvascular pressure. 153 28

The authors studied the clinical and angiographic findings in two patients who had a myocardial bridge (MB) in the right anterior descending coronary artery and did not have any arteriosclerotic lesions in the coronary arteries. The two patients were men, 57 and 58 years old. Both had a history of arterial hypertension (for 19 years and 6 months, respectively) and angina pectoris (for 7 years and 6 months, respectively). The resting EKG showed subepicardial ischemia in one and was normal in the other. The stress test was positive in both. Coronary artery angiography showed an MB in the right anterior descending coronary artery which caused a systolic constriction of 90% and 80%, 3 and 2 cm. long. Both patients had left ventricular hypertrophy. The authors conclude that MB is a frequent cause of coronary insufficiency and that the appearance of symptoms and their severity depends on the degree of systolic constriction, greater than 75%, and on the presence of left ventricular hypertrophy. The majority of patients are controlled with medical treatment and only a small number require surgical therapy.
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PMID:[Myocardial bridging as a cause of coronary insufficiency]. 160 85

The aim of this study was to determine the significance of the "coronary factor" in patients with essential hypertension (EH). Electrocardiogram Holter monitoring was performed in 61 patients with EH stage II (according to the World Health Organization criteria). Silent, ie, painless ST-segment depression, was found in 34 patients on whom echocardiography, a treadmill test, and transesophageal pacing were performed. In 21 patients with EH and silent ischemia, the examination included 201Tl stress scintigraphy, coronary angiography, and a platelet aggregation test. In 15 patients, catecholamines and beta-endorphins were obtained in blood samples during silent ischemia. 201Tl scintigraphy showed transient defects of perfusion without clearance abnormalities (group I) and with clearance abnormalities (group II). The patients in group I had more severe left ventricular hypertrophy (LVH) and a significantly higher platelet aggregation response to 0.5 mumol/L adenosine diphosphate; one patient in this group had coronary atherosclerosis. LVH and the platelet aggregation response was less pronounced in the patients in group II, but atherosclerotic lesions of a coronary artery were observed in four patients. In both groups, norepinephrine and beta-endorphin levels were increased during silent episodes of ischemia. The results suggest that there are different pathogenetic mechanisms of coronary insufficiency in patients with EH, a hypertensive heart, and silent ischemia.
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PMID:Silent myocardial ischemia in patients with essential hypertension. 163 37

Patients with left ventricular hypertrophy (LVH) often exhibit manifestations of myocardial ischemia. In 17 hypertensive patients (group 1, mean age of 56 +/- 4 years, 10 females, 7 males) with ST-segment depression during the exercise electrocardiogram (ECG) and effort angina and normal coronary arteriograms, the left ventricular function at rest and during exercise was studied by heart catheterization. The results were compared with 17 hypertensive patients (group 2, mean age of 56 +/- 6 years, 6 females, 11 males) with coronary artery disease (CAD). The normal pulmonary wedge pressure at rest (group 1, 8.9 +/- 3 mm Hg; group 2, 8.9 +/- 3 mm Hg) was pathologically increased (p less than 0.001) in both groups (group 1, 27.1 +/- 5 mm Hg; group 2, 28.8 +/- 7 mm Hg) even at a work load of 50 W with a further increase at 75 W to 31 +/- 4 and 29.7 +/- 4 mm Hg, respectively. Cardiac output was normal. There was no significant correlation between ST-segment depression, pulmonary wedge pressure, LVH, and Holter ECG. Hypertensive patients without CAD may reveal a disturbed pump function due to ischemia even at low work loads, which does not differ significantly from patients with CAD. This may provoke subendocardial fibrosis and thereby contribute to the development of heart failure.
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PMID:Impaired left ventricular function during exercise in hypertensive patients with normal coronary arteriograms. 171 61

The aim of the study was to analyse electrocardiographic alterations in 30 patients with slight to moderate essential arterial hypertension during the course of hypertensive attacks (DAP greater than 115 mmHg). Standard hematochemical tests were performed in basal conditions, together with 24-h ECG monitoring and an echocardiogram to measure the left ventricular mass index. Echographic monitoring was carried out during hypertensive attacks and for 2 h after the return to basal pressure values. In basal conditions patients showed slight hypopotassemia (23%), left ventricular echographic involvement (57%), left ventricular hypertrophy with or without systolic strain (43%), and ventricular extrasystole (VE) classified as Lown's 1st and 2nd class (17%). During the course of hypertensive attacks, there was a significant increase in systolic strain, the appearance of anterolateral subendocardial ischemia (10%), left anterior hemiblock (3%), lateral subepicardial ischemia (3%), and a marked increase in VE (67%) which were complex in 40% of cases (Lown's classes 3, 4 and 5). A significant correlation was found between the left ventricular mass index and VE/h. The authors stress the multifactorial pathogenesis of echographic alterations and underline left ventricular involvement, acute hemodynamic strain and consequent alterations of coronary perfusion, hypopotassemia, and increased levels of circulating catecholamines.
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PMID:[Electrocardiographic changes in hypertensive emergencies. Their incidence and possible pathogenetic mechanisms]. 172 64

In an attempt to separate the cardiac effects of converting-enzyme (CE) inhibition from those on blood pressure, experiments were performed in rats and dogs with nonantihypertensive (subhypotensive) doses of the CE inhibitor ramipril. (a) Left ventricular hypertrophy: Rats with aortic constriction treated with a nonantihypertensive dose of ramipril (10 micrograms/kg/day) for 6 weeks showed the same prevention and regression of cardiac hypertrophy as groups receiving the antihypertensive dose of 1 mg/kg/day. Comparable results were obtained in animals treated for 1 year. (b) Ischemia-reperfusion injuries: In rats, subchronic oral administration of ramipril in a subhypotensive dose (10 micrograms/kg/day) prevented ex vivo postischemic reperfusion arrhythmias and improved cardiodynamic and metabolic parameters. Almost complete inhibition of cardiac CE was achieved with this low dose. (c) Acute myocardial infarction: Ramiprilat (40 ng/kg/min) was infused for 6 h into the left coronary artery of anesthetized dogs with a ligation of the descending branch of this artery. This route and the low dose were chosen to achieve local cardiac effects without affecting systemic hemodynamics. Ramiprilat significantly reduced the infarct area expressed as a percentage of the area at risk. This cardioprotective effect of ramiprilat was mimicked by bradykinin and abolished by coadministration of a bradykinin antagonist. Thus, factors beyond blood pressure reduction and load changes may add to the cardiovascular benefits of CE inhibitors. This may indicate local (cardiac) paracrine and/or autocrine effects of the renin-angiotensin system and/or participation of kinins.
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PMID:Experimental cardiovascular benefits of angiotensin-converting enzyme inhibitors: beyond blood pressure reduction. 172 38

Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminished flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with beta-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs.
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PMID:New concepts in ischemia prevention. 172 49

Sudden cardiac death (SCD) remains a major unresolved clinical and public health problem, accounting for more than 300,000 of the deaths in the United States annually. The ability to identify potential SCD victims is limited by the large size of the population subgroups that contain the majority of SCD victims and by the apparent time dependence of risk of sudden death. The latter refers to the tendency for SCD to follow other cardiovascular events within a high-risk period of 6-18 months after a primary cardiovascular event, with risk decreasing thereafter. The combination of time dependence and denominator pool size provides a basis for future studies to identify the higher risk individuals. Pathophysiologically, SCD can be viewed as an interaction between structural abnormalities of the heart, transient functional disturbances, and the specific electrophysiological events responsible for fatal arrhythmias. Structural abnormalities provide the anatomic substrate for chronic risk and include the myocardial consequences of coronary artery disease, left ventricular hypertrophy, myopathic ventricles, and specific electrophysiological anatomic abnormalities such as bypass tracts. The functional factors responsible for destabilizing a chronic electrophysiological abnormality include transient ischemia and reperfusion, systemic factors (e.g., electrolyte disturbances, acidosis, and hemodynamic dysfunction), autonomic fluctuations (both systemic and at a tissue level), and myocardial toxic influences such as proarrhythmic effects of various drugs. Each of these changes is able to destabilize myocardial membrane integrity, some regionally and some globally, making the heart susceptible to an electrical triggering event for ventricular tachycardia or fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sudden cardiac death. Structure, function, and time-dependence of risk. 172 1

Cardiovascular diseases are a leading cause of death in end-stage renal disease (ESRD) largely as a result of the progressively increasing age of ESRD patients and the broad constellation of uremia-associated factors that can adversely affect cardiac function. Hypertension, one of the leading causes of renal failure, is a major culprit in this process, causing left ventricular hypertrophy, cardiac chamber dilation, increased left ventricular wall stress, redistribution of coronary blood flow, reduced coronary artery vasodilator reserve, ischemia, myocardial fibrosis, heart failure, and arrhythmias. In addition to impairing the coronary microcirculation, hypertension may contribute to the development of atherosclerotic coronary artery disease, particularly in the presence of the many lipid abnormalities observed in ESRD. These patients have reduced high-density lipoprotein cholesterol and increased plasma triglyceride concentrations, and there is a defect in cholesterol transport. Other abnormalities that may contribute to atherosclerotic coronary artery disease in ESRD are reduced high-density lipoprotein cholesterol synthesis and reduced activity of the reverse cholesterol pathway. Treatment with fibric acids, nicotinic acids, and lovastatin may be useful in lowering cholesterol and triglyceride concentrations in some of these patients. The incidence of coronary artery disease in ESRD populations is difficult to determine. About 25 to 30% of ESRD patients with angina have no evidence of significant coronary artery disease, and an undetermined number have silent coronary disease. The presence of resting electrocardiographic abnormalities caused by hypertension or conduction defects makes it difficult to accurately diagnosis coronary artery disease in ESRD populations by noninvasive methods, including exercise testing and thallium scintigraphy with or without the use of dipyridamole. Hypotension is a frequent complication of the dialytic process. Many factors have been implicated, including autonomic neuropathy. There is no consensus on the function of the efferent limb of the sympathetic nervous system. The afferent limb (arterial baroreflex function) is felt to be impaired. Further, there may be defects in the ability of the cardiovascular system to respond to sympathetic nerve activity. Most studies of autonomic function have used indirect measurements. Studies are underway that use techniques to assess sympathetic function directly. Such experiments with microneuropathy suggest greater skeletal sympathetic muscle discharge in uremic patients than in normal patients.
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PMID:Cardiovascular complications in renal failure. 177 85

A total of 203 patients with hypertension (supine diastolic blood pressure of 100-119 mm Hg) from six centers entered into a 3-week placebo baseline followed by 5 weeks of active treatment (either placebo or isradipine 2.5, 5, 7.5, or 10 mg BID) to determine the effectiveness of isradipine on blood pressure control. Electrocardiographic criteria for left-ventricular ischemia were coded blindly using the Minnesota Codes 4-1 to 4-4 and 5-1 to 5-3 at the end of baseline and active treatment periods. One hundred seventy patients with hypertension and matching and complete electrocardiograms completed the study for analysis: 63 (37%) were white and 117 (69%) were men. They were 52.1 +/- 10.3 years old mean +/- SD; range: 22-77 years). No myocardial infarction occurred during the active phase. Fifty-eight of 170 (34%) at baseline and 54 of 116 (32%) at week 5 had left atrial enlargement. Romhilt-Estes left-ventricular hypertrophy was not significantly different at baseline versus active treatment: 14 of 170 (8.2%) versus 15 of 170 (8.8%). At baseline, the rate of active ischemia was 28.2% (48/170): 27.8% (10/36) were randomized to receive placebo during active treatment and 28.4% (38/134) were given isradipine (P = NS). For those without ischemia at baseline, the rate of change to electrocardiographic ischemia during active treatment was 0% (0/26) for those receiving placebo and 3.1% (3/96) for those taking isradipine (P = NS). For those with ischemia at baseline, the rate of change to no ischemia during active treatment was 20% (2/10) for those receiving placebo and 10.5% (4/38) for those taking isradipine (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of electrocardiographic ischemia in hypertensive patients treated with isradipine or placebo. 182 11


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