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

To test the hypothesis that left ventricular hypertrophy (LVH) may predispose the subendocardium to ischemia, we studied regional myocardial blood flow in dogs with the fibrous ring form of subvalvular aortic stenosis and concentric LVH. Radioactive microspheres, 9 +/- 1 mu in diameter, were used. Eleven dogs with LVH (left ventricular body weight ratio of 6.35 +/- 0.46 gm/kg [mean +/- SEM] and peak left ventricular outflow gradient of 51 +/- 7 mm Hg) were compared to 12 normal dogs (left ventricular/body weight ratio of 3.41 +/- 0.12 gm/kg and peak left ventricular outflow gradient of 6 +/- 3 mm Hg). The two groups of dogs were subjected to comparable experimental interventions including (1) tachycardia produced by atrial pacing (221 +/- 4 beats/min), (2) ascending aortic constriction producing systolic hypertension (212 +/- 5 mm Hg), and (3) creation of an aortic-right atrial fistula lowering diastolic blood pressure (38 +/- 3 mm Hg). Basal regional myocardial blood flow was distributed similarly for LVH and normal dogs (endocardial/epicardial ratio = 0.90 +/- 0.05 and 0.94 +/- 0.03, respectively). During experimental interventions, regional blood flow remained equal to all myocardial layers in normal dogs; however, the endocardial/epicardial ratio diminished in LVH dogs during atrial tachycardia to 0.61 +/- 0.08, during systolic hypertension to 0.68 +/- 0.06, and during diastolic hypotension to 0.50 +/- 0.09. When the diastolic/systolic pressure time index ratio (DPTI/SPTI) was less than 0.8, subendocardial ischemia occurred in dogs with LVH (endocardial/epicardial ratio = 0.66 +/- 0.04) but not in normal dogs (endocardial/epicardial ratio = 0.92 +/- 0.03) (p less than 0.0001). Animals with infracoronary obstruction and LVH demonstrate greater susceptibility to development of subendocardial ischemia for identical hemodynamic interventions than do normal animals.
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PMID:Regional myocardial blood flow in left ventricular hypertrophy. An experimental investigation in Newfoundland dogs with congenital subaortic stenosis. 621 74

In order to perform intracardiac repair safely during aortic cross clamping, we designed this study to evaluate the protective effect of coenzyme Q10 (CoQ10) on hypertrophied ischemic myocardium from the aspect of energy metabolism. Six to nine months preceding the study, aortic bandings were carried out on 14 puppies to produce left ventricular hypertrophy (LVH). These dogs with LVH were then subjected to total cardiopulmonary bypass and were evenly divided into control and CoQ10-treated groups (10 mg/kg of intravenous administration plus 1 mg/kg per hr of intracoronary injection). Myocardial ischemia was induced by aortic cross clamping for 2 hr under moderate systemic hypothermia. The results indicated that the administration of CoQ10 had a protective effect on hypertrophied ischemic myocardium, since depletion of high-energy phosphate (HEP) was uniformly prevented, and accumulation of lactate was simultaneously decreased during the 2 hr of aortic cross clamping. On the other hand, there were marked exhaustion of HEP and rapid increase in lactate following the 2 hr of ischemia in the control group, these being much more predominant in the subendocardial layer.
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PMID:Effect of coenzyme Q10 on hypertrophied ischemic myocardium during aortic cross clamping for 2 hr, from the aspect of energy metabolism. 622 44

The quantitative VCG criteria (VCGer) for left ventricular hypertrophy (LVH) and their diagnostic power were determined in 165 hypertensive men and 86 women over 40 years of age without congestive cardiac failure in comparison with 91 normal men and 108 normal women. The patients were grouped according to the presence or absence of LVH determined by X-ray (men: 96 without and 69 with LVH, women: 41 without and 45 with LVH). The proper statistical methods were used taking into account whether their distributions were symmetrical or asymmetrical. We found some sex differences of VCG criteria. The most striking results were the lack of increased voltage, and the great sensitivity of the orientation of Q vectors to the left (Q left). Q left may be induced by: 1. a septal hypertrophy, alone or accompanied by a hypertrophy of the anterior and posterior paraseptal regions of LV wall, 2. by a subendocardial ischemia at these levels induced by the increase of intraventricular pressure, 3. by possible spatial change of the septum, 4. by all these factors acting synchronously, 5. by other, unknown factors. These VCGcr for LVH found by us are different from those in the literature, but they are valid in Romania.
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PMID:Absence of increased cardiac voltage and the importance of Q vectors for the diagnosis of left ventricular hypertrophy in early stages of hypertension in patients over 40 years of age. 623 49

The electrocardiogram (ECG) of athletes reflects physiologic cardiovascular adaptations that occur in well-conditioned individuals. To more clearly define electrocardiographic changes seen in predominantly power-trained athletes, the ECGs of 289 apparently healthy professional football players were analyzed in detail. The players, aged 21 to 35 years, one-third of whom were black, had a mean body surface area of 2.24 m2, a mean heart rate at rest of 56 +/- 9 beats/min (with 77% (223) having a rate of less than 60 beats/min), and a mean P axis of 30 +/- 25 degrees. A wide QRS-T angle (greater than 60 degrees) was present in 14% (41 players) of the group. The mean PR interval was 0.18 +/- 0.02 second (greater than 0.21 in 9% [26 players]). Although two-thirds of the players had a QRS duration of 0.10 second, only 1 had right bundle branch block and none had left bundle branch block. The sum of S in lead V1 plus R in lead V5 averaged 37 +/- 9 mm, with 35% (101 players) demonstrating voltage criteria for left ventricular hypertrophy. The S + R value varied inversely with weight (r = -0.27, p less than 0.002). The maximum T height in any lead had a mean of 8.6 +/- 3 mm, with 22% (64 players) having a T height greater than or equal to 11 mm. U waves were universally present. ST-T changes mimicking ischemia were noted in 39 of 289 players (13%), 22 (58%) of whom were black (p less than 0.001). The maximal J-point elevation in any lead averaged 1.9 +/- 0.9 mm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrocardiogram of the athlete: an analysis of 289 professional football players. 623 51

Alterations in ventricular diastolic properties are commonly seen in the diseased heart, and have been extensively studied in coronary artery disease, congestive cardiomyopathy, and left ventricular hypertrophy due to pressure or volume overload. Acute increases in left ventricular (LV) diastolic pressure relative to volume occur regularly during the transient ischemia of angina pectoris and may contribute to the dyspnea and pulmonary congestion that commonly accompany this condition. Although the mechanism of this altered disastolic distensibility is debated, a substantial body of evidence favors a role for residual diastolic interaction between contractile elements in the ischemic heart. Congestive cardiomyopathy also appears to be associated with increased LV diastolic stiffness. While this may in part be related to fibrosis of the LV wall, shifts of the abnormal diastolic pressure-volume relation toward normal have been reported with sodium nitroprusside infusion or the beta-adrenergic agonist salbutamol, suggesting important contribution of physiologic factors to the increased resting LV stiffness in this condition. LV hypertrophy (LVH) is associated with increased effective diastolic chamber stiffness, but normalized LV diastolic stiffness is increased only in LVH due to chronic pressure overload. Possible explanations for these findings are discussed.
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PMID:Diastolic pressure-volume relations in the diseased heart. 644 88

The research showed a high incidence of electrocardiographic signs of hypertrophy of the right ventricle of the heart under high-altitude conditions. Code 2-3 was found in 49.2% of highlanders examined, code 2-4 in 1.5%, code 3-2 in 17.0%, and code 9-4-2 in 54.4%. Some cases of hypertrophy of the right ventricle of the heart (code 3-2, approximately 4-5%) are attended by disturbances in the repolarization processes in the right chest electrocardiographic leads (code 5-1 or 5-2). According to the interpretations of the Minnesota code, these shifts should be considered ischemic. But information yielded by the Rouz questionnaire, the results of clinical examination, and tests with maximum physical load in 8 persons who had such shifts on the ECG did not confirm the presence of symptoms of ischemic heart disease. That is why changes in T wave detected in highland aborigenes with marked right-ventricular hypertrophy but no clinical symptoms of ischemic heart disease should be accepted as evidence of ischemia. Otherwise, if the disturbances in the repolarization processes are interpreted as signs of myocardial ischemia, the prevalence of ischemic heart disease among the population of the highlands may be overestimated. The introductin of restriction in relation to code 3-2 when it is combined with code 5-1 or 5-2 will make it possible to study more exactly the true prevalence of ischemic heart disease in the presence of hypertrophy of the right ventricle of the heart.
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PMID:[Interpretation of the ECG changes using the Minnesota code in the presence of right-ventricular (high-altitude) cardiac hypertrophy]. 644 10

Left-sided congestive heart failure may be secondary to decreased left ventricular myocardial compliance in some patients. To investigate the anatomic basis for altered wall stiffness, morphometric determinations of muscle cell nuclear density and percent of myocardium consisting of muscle cells were made for right and left ventricular free wall and septum in 127 hearts with normal coronary arteries. The hearts were normal (33 patients), had left ventricular hypertrophy (28 patients), right ventricular hypertrophy (25 patients), or chronic dilatation (41 patients). With cardiac enlargement, the average percent of myocardium consisting of muscle did not change from the approximately 75% value characteristic of normal hearts. In contrast, muscle cell nuclear density decreased proportionate to cardiac enlargement, demonstrating that muscle cell hypertrophy, not hyperplasia, is the basis for weight increase. Some hearts with marked longstanding dilatation also had perivascular and interstitital "striae" of connective tissue differing from replacement fibrosis. An increase in epicardial coronary artery caliber commensurate with increased heart weight suggests that ischemia is not the basis of connective tissue increase. The results show that cardiac muscle cell hypertrophy is accompanied by commensurate increase in interstitial connective tissues. This pattern of myocardial growth with cardiac enlargement may produce increased myocardial stiffness simply as a result of increased wall thickness, and may lead to left-sided congestive heart failure.
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PMID:Constituents of the human ventricular myocardium: connective tissue hyperplasia accompanying muscular hypertrophy. 644 58

Chronic hypertension increases the risk of myocardial infarction and the morbidity and mortality associated with it. Although accelerated atherosclerosis is partially responsible, other abnormalities in the coronary circulation associated with hypertension, such as decreased coronary vascular capacity and capillary density, could also contribute. To evaluate the effects of these nonatherosclerotic abnormalities, we produced sudden coronary occlusion in nine chronically hypertensive dogs. The mean aortic pressure and left ventricular mass were about 50% greater in hypertensive dogs than in the nine controls. Before occlusion and 5 min and 49 h after occlusion, myocardial blood flow was measured with tracer microspheres. Also, the extent of infarction in selected myocardial segments was quantified histologically. We found that coronary occlusion reduced flows to a similar extent, and that, over a 48-h period, collateral flow increased to a similar extent in the two groups. In addition, the amount of necrosis associated with a given degree of ischemia was similar in the two groups. Although the extent of the left ventricle that became ischemic was greater in the hypertensive dogs (28 +/- 2 vs. 18 +/- 4%; P < 0.05), chronic hypertension and left ventricular hypertrophy did not limit the recruitment of collateral supply or increase the amount of necrosis associated with a given degree of ischemia.
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PMID:Myocardial infarction in dogs with chronic hypertension and left ventricular hypertrophy. 644 77

Using a canine model of subcoronary valvular aortic stenosis, we determined myocardial blood flow, high-energy phosphate content, and mitochondrial function in eight hearts with chronic left ventricular hypertrophy. Fourteen normal hearts were used for control data. Myocardial blood flow was determined by injection of tracer microspheres. During cardiopulmonary bypass, left ventricular transmural biopsy specimens were taken for metabolic analyses. Subepicardial and subendocardial content of adenosine triphosphate (ATP) and creatine phosphate (CP) were assayed. Respiratory control indices for isolated mitochondria were measured by use of NAD-linked and FAD-linked substrates. Endocardial blood flow, subendocardial high-energy phosphate content, and respiratory control indices for NAD-linked substrate in the hearts with chronic left ventricular hypertrophy were significantly lower than the normal values. These data provide insight into the metabolic and myocardial blood flow abnormalities occurring in cardiac hypertrophy and provide a framework for understanding the altered response of hypertrophied hearts to ischemia.
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PMID:Characteristics of chronic left ventricular hypertrophy induced by subcoronary valvular aortic stenosis. I. Myocardial blood flow and metabolism. 645 Aug 57

The increased susceptibility of hearts with chronic left ventricular hypertrophy (CLVH) to damage during ischemia has been suggested but not documented. The purpose of this study was to isolate ischemic events in hearts with CLVH from reperfusion events. Using physiological and biochemical parameters, we compared the rate and extent of myocardial injury during ischemic contracture between eight canine hearts with CLVH induced by subcoronary valvular aortic stenosis and 14 normal canine hearts. Preischemic myocardial blood flow was determined by injection of tracer microspheres. During cardiopulmonary bypass, each heart was instrumented with a left ventricular balloon and made globally ischemic. At control, contracture initiation, and contracture completion left ventricular transmural biopsy specimens were assayed for subepicardial and subendocardial adenosine triphosphate (ATP) and creatine phosphate (CP). Mitochondrial respiratory control indices for NAD-linked and FAD-linked substrates were measured. Preischemic endocardial blood flow in hearts with CLVH was significantly lower than in normal hearts. At control, subendocardial ATP and CP and the respiratory control index for NAD-linked substrate were significantly lower in hearts with CLVH than in normal hearts. Hearts with CLVH reached contracture initiation significantly sooner than normal hearts. All hearts demonstrated significant decreases in high-energy phosphate content and mitochondrial function during ischemia. Reperfusion injury notwithstanding, we concluded that hearts wih CLVH are more susceptible to ischemic injury than are normal hearts, perhaps related to lower endocardial blood flow, lower subendocardial high-energy phosphate stores, and depressed mitochondrial function prior to ischemia.
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PMID:Characteristics of chronic left ventricular hypertrophy induced by subcoronary valvular aortic stenosis. II. Response to ischemia. 645 Aug 58


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