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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sudden death accounts for about 15-20% of all natural fatalities in the industrially developed world. Most of the victims have a substrate of extensive myocardial injury caused by coronary heart disease, cardiomyopathy and hypertensive heart disease. In most cases, the immediate cause of death is triggered by ventricular tachycardia which degenerates into ventricular fibrillation. Changes in myocardial electrical properties may be critically modified by ischemia, imbalance in the autonomic nervous system, electrolytic disorders, and haemodynamic factors. We review the causes of sudden cardiac death, giving special attention to the effect of beta-adrenoceptor blockade as a preventive measure.
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PMID:[Sudden cardiac death. Significance of beta blockaders]. 135 74

To determine whether myocardial ischemia is accompanied by variation in heart rate and/or blood pressure, ST-segment analysis on Holter-ECG and ambulatory blood pressure monitoring was performed in 78 patients (64 males/14 females) with essential hypertension. Thirteen out of 55 patients (24%) with angiographically proven coronary artery disease (CAD) showed ST-segment depression (ST-D; group A pos). We observed 41 ST-D (1-11 ST-D; median: 2) lasting from 1 min to 70 min 15 s (median: 4 min 42 s) and an average depression of 185 +/- 48 mV. In comparison, in 6 of 23 patients (26%) with a normal angiogram 24 ST-D (1-10; median: 3; group B pos), which showed longer duration (1 min to 109 min 20 s; median: 11 min 10 s) and less depression (137 +/- 47 mV) have been found. 73.3% of all ST-D in group A pos and all in group B pos were preceded by an average increase in heart rate of 13 bpm. Exclusively, 12 episodes of ischemia (29.3%) in patients with CAD and 8 (33.3%) in patients without CAD were accompanied by an increase in blood pressure, which was more distinct in group A pos. Transient myocardial ischemia can be shown in hypertensive heart disease unrelated to CAD. A clear correlation between an increase in blood pressure and ST-D could not be proven.
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PMID:[Blood pressure variability and transient myocardial ischemia in patients with essential hypertension]. 151 10

The operating characteristics of thallium stress testing for detection of significant epicardial coronary artery disease (CAD) in hypertensive subjects with chest pain or electrocardiographic (ECG) ischemia have not been previously defined. This becomes important because of the high prevalence of both hypertensive heart disease and CAD. Ninety-two hypertensives with a history of typical or atypical chest pain or ECG myocardial ischemia underwent coronary arteriography, 2D-guided echocardiography, and thallium-201 stress testing, combined with intravenous dipyridamole if the rate-pressure product was less than 20,000. Patients with myocardial infarction, prior revascularization procedure, valvular heart disease, and chronic ethanol abuse were excluded. The mean age was 54.8 +/- 9.9 years with 55% blacks and 46% women. Eighteen patients (19.6%) had significant (greater than or equal to 50% luminal diameter narrowing) epicardial CAD at catheterization, of whom 17 had positive thallium scans. Overall, there were 17 true positives, 47 true negatives, 27 false positives, and one false negative resulting in 94.4 +/- 5.4% sensitivity (95% confidence limits [95% CL] 71 to 100%), 63.5 +/- 5.6% specificity (95% CL 51 to 74%), 38.6 +/- 7.3% positive predictive value (95% CL 25 to 54%), 97.9 +/- 2.1% negative predictive value (95% CL 88 to 100%), and 69.6 +/- 4.8% overall accuracy (95% CL 59 to 79%). For hypertensive patients with chest pain or ECG myocardial ischemia, the high sensitivity and negative predictive value and low false negative rate support the role of thallium stress testing +/- dipyridamole as an exclusion test for significant CAD.
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PMID:A negative thallium (+/- dipyridamole) stress test excludes significant obstructive epicardial coronary artery disease in hypertensive patients. 153 15

Left ventricular hypertrophy (LVH) constitutes a powerful independent risk factor in hypertensive heart disease. Although initially the wall stress, i.e., left ventricular afterload, remains normal, the coronary reserve is diminished due to disturbances in the microcirculation. This is also shown in the commonly present silent ischemia episodes in Holter monitoring. LVH also causes ventricular dilation and heart failure. Apart from systolic wall stress LVH is modulated by the trophic effects of the sympathetic nervous system and angiotensin II and genetic factors. Long-term antihypertensive treatment must therefore focus on regression of both LVH and the microvascular abnormalities. A step approach for the treatment of the LVH has been recommended on the basis of the experience of this working group with calcium antagonists and ACE inhibitors, whereas the place of beta-blockers is as yet unclear. Preliminary data indicate that coronary flow rescue can also be improved after chronic antihypertensive treatment.
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PMID:Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs. 153 67

In essential hypertension, ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal, even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). One of the profound mechanisms influencing both myocardial and coronary function in hypertensive heart disease is the pressure-dependent development of smooth vascular hypertrophy (media) or coronary resistance vessels. Consequently, the oxygen supply to the myocardium is impaired and secondary lesions occur such as fibrosis, increased myocardial and perivascular collagen content and scars within the heart muscle. Diastolic dysfunction develops, as well as an increase in myocardial stiffness, thus promoting the transition from the concentric (compensated) to the eccentric or dilated (decompensated) state, with the consequence of the occurrence of cardiac failure. On the basis of both functional and morphological criteria, evidence is presented in this report that coronary small vessel disease is one of the underlying mechanism for the development of cardiac failure in hypertensive heart disease.
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PMID:Development of cardiac failure by coronary small vessel disease in hypertensive heart disease? 183 64

Left ventricular hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. There are multiple mechanisms in which left ventricular hypertrophy may account for this excess mortality including increased incidence of arrhythmias, systolic an diastolic dysfunction, relative ischemia, and associated coronary artery disease. Diastolic dysfunction, manifested by reduced ventricular distensibility of the hypertrophic left ventricle, appears to be an early characteristic of the hypertensive heart since echocardiographic techniques have demonstrated diastolic filling abnormalities in untreated essential hypertensives even before significant left ventricular hypertrophy appears. The presence of left ventricular hypertrophy is difficult to detect by electrocardiography. Echocardiography seems to be the best non-invasive method for the detection of hypertensive heart disease: it shows early abnormalities of left ventricular compliance, frequently left ventricular hypertrophy and late abnormalities of myocardial contractility.
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PMID:[Heart effect of arterial hypertension. Heart hypertrophy as a risk factor. Study technics (electrocardiogram, echocardiography, exercise test and Holter]. 213 76

In hypertensive heart disease without coronary artery disease it has been proposed that the presence of ischemia of myocardial tissue is due to an inadequate increment of myocardial mass or to an increase in coronary artery resistance. In this study, 18 patients with aortic stenosis, without coronary artery disease were included. It was demonstrated that the existence of myocardial ischemic, induced by atrial pacing and manifested by ST segment depression, had direct association to increased myocardial mass, and it had no relation with left ventricular telediastolic pressure nor with transvalvular gradient. The results support the hypothesis that an inappropriate increment of the myocardial mass is the main cause of myocardial ischemia in these type of cardiopathies.
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PMID:[Myocardial ischemia in aortic stenosis]. 253 25

Despite recent declines in mortality from coronary heart disease (CHD), it remains the major cause of death in the United States for blacks and whites. Although the prevalence of the ischemic syndromes in blacks and whites is similar, cardiac mortality and sudden cardiac death rate are higher in blacks. Recent attempts to explain the excess mortality in blacks have focused on barriers to health care and on sociocultural differences in perceptions of and responses to symptoms of CHD. However, the anatomic substrates of ischemia and sudden cardiac death are also different in blacks and whites. Obstructive coronary artery disease tends to be more severe in whites, while blacks have a greater prevalence of hypertensive heart disease. A body of evidence has recently emerged showing that the presence of left ventricular hypertrophy (LVH) is an important, potent predictor for subsequent cardiac death and that the mortality risk of LVH may be particularly high when underlying coronary disease is present. The greater prevalence and severity of hypertension and LVH in blacks may explain the higher cardiac mortality in blacks, even in the presence of less severe coronary disease. The reason why mortality risk is increased in the presence of LVH has not been established. Evidence suggests that it may be due to the increased predisposition to malignant arrhythmias and the increased frequency of potentially lethal silent ischemic events that occur in hypertensive individuals, particularly those with LVH.
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PMID:Anatomic substrate differences between black and white victims of sudden cardiac death: hypertension, coronary artery disease, or both? 262 Apr 68

In essential hypertension ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). Digitalis glycosides, together with antihypertensive measures, are indicated for the dilated hypertensive heart; beta-receptor blockers are sound medication for the compensated hypertensive heart both with and without coronary stenoses. The following discussion includes classification of hypertensive heart disease based on the cardiac complications following hypertension.
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PMID:Functional dynamics of the left ventricle in hypertensive hypertrophy and failure. 624 Apr 52

This study was designed to assess left ventricular contractility in hypertensive patients with normal coronary angiography and anginal pain. An abnormally high percentage of hypertensive patients (approximately 30%) undergoing cardiac catheterization because of anginal pain and/or exercise-induced ST-segment depressions has angiographically normal coronary arteries. Possible reasons for these signs of ischemia include a microvasculopathy, metabolic abnormalities and an increased oxygen consumption as a result of left ventricular hypercontractility which was studied here. Left ventricular volumes and ejection fraction were determined in 50 patients with arterial hypertension (23 men, 27 women, age 60 +/- 8 years, RR 154 +/- 24/91 +/- 12 mm Hg) by cardiac catheterization and computerized analysis of laevocardiographies. The control group were 50 normotensives (30 men, 20 women, age 57 +/- 12 years, RR 128 +/- 12/76 +/- 8 mm Hg) without coronary artery disease. The angiographical data were correlated with age, sex. ECG, echocardiography, laboratory findings, medication and duration of hypertension. The left ventricular ejection fraction was significantly increased in the group of hypertensives (75.8 +/- 6.3 vs. 67.7 +/- 5.0%, p < 0.001). This difference was mainly due to a significantly reduced endsystolic left ventricular volume (37.1 +/- 15.3 vs. 47.7 +/- 10.8 ml, p < 0.001); enddiastolic left ventricular volume was not significantly different (140.5 +/- 26.8 vs. 149.0 +/- 27.5 ml, p > 0.1). A hyposystolic form of hypertensive heart disease was not observed in this group of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular hypercontractility in hypertensive patients with anginal pain and normal coronary angiograms. 757 66


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