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

Chronic right ventricular hypertrophy (RVH) has been shown to produce changes in left ventricular diastolic properties but minimal effects on left ventricular systolic function. We studied the effects of chronic pressure overload RVH on left ventricular systolic function before and after reversible hypothermic global ischemia. RVH was induced by pulmonary artery banding (PAB) in newborn piglets (5 to 7 days). At 2 months of age the PAB group (n = 6) and a control group (n = 8) were subjected to cardiac arrest on cardiopulmonary bypass with cold crystalloid cardioplegia (10 degrees C) for 2 hr and were reperfused for 1 hr. Left ventricular function was assessed by a conductance catheter in the left ventricle measuring the end-systolic pressure-volume relationship (Emax). Preischemic and postischemic Emax were the same in the control group (4.1 +/- 0.4 mm Hg/ml before vs 4.1 +/- 0.4 mm Hg/ml after ischemia), but significantly different in the PAB group (4.7 +/- 0.5 mm Hg/ml before vs 2.97 +/- 0.7 mm Hg/ml after ischemia, p less than .05). There also was a marked drop in ATP and phosphocreatine (CP) content in the PAB group during ischemia (ATP, 20 +/- 2 mmol/kg dry wt before vs 10 +/- 2 mmol/kg dry wt after ischemia, p less than .05; PC, 26 +/- 3 mmol/kg dry wt before vs 11 +/- 1 mmol/kg dry wt after ischemia, p less than .05). In the control group there was no change in ATP content and, although CP did drop by end-ischemia, there was complete recovery by 1 hr of reperfusion but minimal CP recovery in the PAB group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired left ventricular postischemic function and metabolism in chronic right ventricular hypertrophy. 295 97

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). Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption. Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine, enalapril, and nifedipine) were analyzed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers and angiotensin-converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy. No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Comparative analysis of cardiac function, geometry, energetics and coronary reserve in hypertensive heart disease. 296 4

During the initial phase of the World Health Organization (WHO) "Community Control Program of Hypertension" in Italy, 1190 subjects with high blood pressure derived from a general population random sample (5856 people of both sexes, aged 20 to 64 years) were enrolled in a hypertension register. At the registration visit (RV), each of them gave case history details and underwent a complete clinical examination, blood and urine tests, and a standard 12-lead electrocardiogram (ECG). All the ECGs were read by a single coder, using the second version of the Minnesota Code (MC). We calculated the prevalence of electrocardiographic codes according to sex, age, and the state of antihypertensive treatment. The overall prevalence of electrocardiographic abnormalities (i.e., all codes except 1:0 and isolated 9:4) was 40.8% with a slightly higher prevalence in males than in females: 42.4% versus 39.4%. Codes related to left ventricular hypertrophy (LVH) (3:1 or 3:3) were also more frequent in males (21.2%) than in females (14.5%) but not those related to ischemia (4:1-4:3 or 5:1-5:3). In fact, group 4 codes were present in 4.0% of males and 16.1% of females; group 5 codes, in 5.7% of males and 18.1% of females. Abnormal codes generally increased with increasing age, but those related to LVH did not follow this general rule in males. In fact, in the age class 20-29 years, codes 3:1 were found in 11.1% and codes 3:3 in 17.5% of the subjects, whereas the corresponding frequencies in the oldest age group (60-64 years) were 15.2% and 12.4%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrocardiographic findings in hypertensive patients of a population sample. Role of sex, age, and antihypertensive treatment. 296 37

The present study was designed to examine the effects of two new angiotensin-converting enzyme (ACE) inhibitors, CGS 14831 and CGS 16617 (3 mg/kg i. v. 1 min prior to occlusion and 4 and 24 h after occlusion), on myocardial ischemic (MI) damage and left-ventricular hypertrophy in rats. Administration of CGS 14831 or CGS 16617 inhibited angio-tensin-I-induced pressor responses by 40-100% for 4 h after each dose. Myocardial creatine phosphokinase (CK) levels were 10.6 +/- 0.6 U/mg protein in sham-MI animals, and following coronary artery occlusion for 48 h were decreased to 4.1 +/- 0.2 U/mg protein in MI + vehicle animals (p less than 0.01). CGS 14831 and CGS 16617 attenuated the decrease in CK content and resulted in 47 and 40% sparing, respectively, of the left-ventricular free wall. Neither agent attenuated the left-ventricular hypertrophy which developed following coronary artery occlusion. These data indicate that the nonsulfhydryl ACE inhibitors CGS 14831 and CGS 16617 have a significant cardioprotective effect in rats surviving 48 h, and suggest a potential therapeutic usefulness of these agents for the treatment of ischemia-induced heart failure.
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PMID:Effects of two nonsulfhydryl angiotensin-converting enzyme inhibitors, CGS 14831 and CGS 16617, on myocardial damage and left-ventricular hypertrophy following coronary artery occlusion in the rat. 297 11

The quality of myocardial protection during cardiac arrest in cardiac operations was investigated in 310 patients. Eighty patients underwent aortic valve replacement and 230 had coronary artery bypass grafting. Four different cardioplegic solutions (Kirsch, Bretschneider, St. Thomas' Hospital, and Hamburg) and the method of induced fibrillation were tested by ultrastructural analysis of the degree of ischemic injury at the end of the cardiac arrest period. Hypothermia was identical in all five groups. In this study, subendocardial and subepicardial needle biopsies were evaluated by a standardized scoring system. Chemical cardioplegia produced mainly moderate ultrastructural injury independent of the time of ischemia. Kirsch cardioplegia and the intermittent fibrillation procedure produced ischemic injury of greater and unpredictable severity. Only with Kirsch cardioplegia was a correlation observed between the duration of intraoperative arrest and the degree of injury, which is indicative of a lack of myocardial protection. The tolerance to ischemia was significantly better in patients undergoing bypass grafting than in those with aortic valve disease and therefore longstanding hypertrophy. In conclusion, the Bretschneider, St. Thomas' Hospital, and Hamburg solutions provide satisfactory myocardial protection but are not able to completely prevent myocardial ischemic injury. Kirsch cardioplegia and the intermittent fibrillation procedure provide insufficient myocardial protection. Patients with left ventricular hypertrophy are at a greater risk during cardiac operations than patients undergoing coronary bypass operations.
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PMID:Ultrastructural study comparing the efficacy of five different methods of intraoperative myocardial protection in the human heart. 308 35

The effect of hypertension, hyperlipidemia, and the combination of both on acute and chronic myocardial ischemia were evaluated in a total of 30 male rabbits. After preliminary hypertension and/or hyperlipidemic load by loading of the abdominal aorta and/or cholesterol feeding, acute ischemia was produced by clipping of the left coronary artery. The banding produced elevation of carotid arterial pressure and left ventricular hypertrophy. Cholesterol feeding resulted in severe atheromatous changes in all sizes of coronary arteries. The intimal thickening was due to foam cell accumulation in all arteries examined. Animals pretreated with the combination of hypertension and hyperlipidemia displayed the most severe cardiolmegaly with advanced coronary atherosclerosis and chronic ischemic lesions of the myocardium, i.e., perivascular patchy fibrosis in the subendocardial area. Furthermore, electron microscopic detection of ultrastructural myocardial damage, involving glycogen depletion, sarcoplasmic edema, mitochondrial swelling, and contractile abnormalities, was also most frequent in this group. These changes were quantitated using the ischemic score. These results confirm the hypothesis that fatal ischemic injuries may occur clinically in human hearts with coronary insufficiency due to coexistence of hypertensive cardiomegaly and severe coronary atherosclerosis. They offer a model for further study of these combined effects.
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PMID:An ultrastructural study on ischemic lesions in rabbits' hearts with pressure overload and hyperlipidemia. 315 60

We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of cardiac hypertrophy on the coronary collateral circulation. 315 52

To assess the significance and accuracy of noninvasive tests in detecting significant coronary artery disease (CAD; greater than 50% stenosis), the Master's exercise test, treadmill exercise test and dipyridamole-loading myocardial perfusion scintigraphy were performed and their results were compared with coronary angiographic findings in 60 patients with angina but without myocardial infarction. Among these, 27 patients had significant CAD. The Master's test performed in outpatient clinics had an 85% sensitivity and a 76% specificity in detecting significant CAD, when the degree of ST depression was equal to or exceeded 1 mm. The sensitivity further improved to 96% by adding chest pain to the criteria; then all patients with multivessel disease or critical ischemia were identified by the Master's test. Treadmill tests performed after admission had a 78% sensitivity and a 67% specificity. When the severity of ischemia was judged either by exercise capacity or the degree of ST depression or the coronary T wave, the treadmill test was superior to the Master's test. Although patients without significant CAD had longer exercise capacity and the higher maximum heart rate in the treadmill test than did those in the Master's test, these trends were similar but less marked in patients with significant CAD. Dipyridamole-loading myocardial perfusion scintigraphy showed an excellent sensitivity and specificity; 96% and 94%, respectively, in detecting significant CAD. It was particularly useful in distinguishing false positive exercise results due to left ventricular hypertrophy and coronary spasm and that in women, from true positive results. In conclusion, the Master's test is a simple and useful method for screening CAD in community hospitals and in outpatient clinics.
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PMID:[Accuracy of the Master's exercise test in detecting significant coronary artery disease]. 326 34

While the total ischemic burden on the left ventricle represents the combined effects of both symptomatic and asymptomatic myocardial ischemia, the total vascular burden has many components including an increased systemic peripheral vascular resistance, an increased pulmonary vascular resistance, and an increased coronary vascular resistance. These factors may all influence ventricular function. Hypertension contributes significantly to the vascular burden, especially when combined with left ventricular hypertrophy, which predisposes to ischemia by multiple mechanisms. In patients with hypertension and cardiomegaly, sublingual nifedipine has been shown to increase left ventricular (LV) ejection fraction and the average diastolic filling rate. In the presence of acute myocardial infarction, nifedipine moves the LV function curve onto a better Frank-Starling relationship as pulmonary wedge pressure falls or stays the same and cardiac output rises. However, because of the delicate balance between myocardial perfusion and the benefits of afterload reduction, including improved remodelling, nifedipine should be given only to selected patients. In congestive heart failure, low-dose nifedipine reduces the afterload and has been shown to have beneficial effects in the majority of patients. Two specific adverse outcomes in only two patients have been reported, one with initial hypotension and one given high-dose nifedipine. Combination nifedipine-beta blocker therapy has been shown to be favorable in the treatment of all varieties of angina, hypertension, and hypertrophic cardiomyopathy. Therefore, when administered appropriately, nifedipine reduces the total vascular burden on the heart in a variety of cardiovascular diseases, with consequent improvement in LV function and a diminished threat of potential myocardial ischemia.
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PMID:The total vascular burden, peripheral and coronary: vasodilator effects of nifedipine. 327 10

Atherogenic traits, living habits, signs of preclinical disease, and susceptibility all contribute to cardiovascular disease. High low-density lipoprotein is positively related to coronary heart disease, and high high-density lipoprotein is inversely related. Systolic or diastolic hypertension at any age in either sex contributes powerfully. The impact of diabetes is greater for women and varies with the number of accompanying risk factors. High-normal fibrinogen values further escalate risk of these atherogenic factors. An atherogenic life-style is typified by a diet excessive in fat, calories, and salt; sedentary habits; unrestrained weight gain; and cigarette smoking. Moderate alcohol use may be beneficial. Use of oral contraceptives beyond age 35 years and in conjunction with cigarette smoking predisposes one to thromboembolism. Type A behavior carries an increased risk, and men married to more highly educated women and to women in white-collar jobs are more vulnerable. Signs of preclinical ischemia include silent myocardial infarction, left ventricular hypertrophy on ECG, blocked intraventricular conduction, and repolarization abnormalities. Measures of innate susceptibility include a family history of early cardiovascular disease. Quantitative combination of risk factors provides optimal prediction, including persons with multiple marginal abnormalities. Preventive management should also be multifactorial and requires a commitment to behavior modification and alteration in life-style.
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PMID:New perspectives on cardiovascular risk factors. 330 Feb 33


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