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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 investigate the clinically important but controversial question of how hypertension during coronary occlusion affects infarct size 24 pigs underwent 1 h occlusion of the mid left anterior descending coronary artery and 24 h reperfusion and were randomised to one of three treatment groups. In group 1 blood pressure was increased during the occlusion period by an infusion of methoxamine; in group 2 tachycardia was induced by atrial pacing; and in group 3 no intervention was performed. The area at risk and infarct size were quantified by digital planimetry of slices of myocardium previously marked with fluorescein and with triphenyl-tetrazolium. Methoxamine maintained mean aortic blood pressure at 117 (SEM8) mmHg during occlusion, whereas the values were 80(6) mmHg in group 2 and 67(9) mmHg in group 3. Pacing increased heart rate to 146(1) beats.min-1 in group 2; it was 103(5) in group 1 and 99(8) in group 3. The pressure-rate product achieved was similar in groups 1 and 2 and significantly higher than in group 3. The pathological studies showed infarct size to be moderately but significantly larger in group 1 (14[3.5]% of the left ventricle) and similar in groups 2 (10.5[3.9]%) and 3 (10.1[2.2]%). The ratio of infarct size to area at risk was also significantly higher (0.743[0.057]) in group 1 with no differences between group 2 (0.604[0.055]) and group 3 (0.613[0.027]). At similar pressure-rate product, infarct size was thus greater with hypertension but not with pacing alone, showing a deleterious effect of increasing blood pressure in this experimental model with negligible collateral blood flow.
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PMID:Influence of tachycardia and arterial hypertension on infarct size in the pig. 324 33

When acute myocardial infarction occurs in patients with hypertension and left ventricular hypertrophy (LVH), the incidence of sudden cardiac death increases markedly. Possible explanations include increased size of the occluded vascular bed secondary to more extensive atherosclerotic coronary vascular disease in the presence of hypertension, decreased coronary reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in hypertrophied cardiac muscle. To explore these possibilities, we produced acute circumflex coronary occlusion during the resting, conscious state in 32 control dogs and in 28 dogs with hypertensive LVH. Before coronary occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and 125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and 32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less than 0.01 vs control). The perfusion fields of the occluded vessel defined by postmortem coronary angiography were similar in the two groups (31 +/- 2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH). Thus, the increased incidence of sudden cardiac death after coronary artery occlusion in hypertensive LVH dogs cannot be explained by increased size of the occluded vascular bed and is probably related to the decreased coronary reserve or intrinsic electrophysiologic abnormalities that characterize pressure-induced hypertrophied cardiac muscle.
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PMID:Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs. 621 Apr 60

Myocardial ischemia is frequently observed in patients with cardiac hypertrophy even when the conduit coronary arteries are normal. Recent studies indicate that impaired coronary reserve in hypertrophied hearts probably occurs because growth of the coronary bed does not keep pace with increases in cardiac mass. The imbalance between vascular proliferation and muscle growth is probably most severe when cardiac hypertrophy is produced by pressure overload. Experimental studies also suggest that abnormalities intrinsic to pressure-hypertrophied heart muscle (decreased capillary density; decreased coronary reserve; electrophysiologic abnormalities) adversely affect the response of the enlarged heart to sudden coronary occlusion. When animals with hypertension and left ventricular hypertrophy are subjected to sudden coronary occlusion, the incidence of sudden cardiac death is increased severalfold and infarct size is substantially augmented. These observations suggest that abnormalities in the coronary microcirculation that accompany cardiac hypertrophy play a significant role in the pathogenesis of the complications associated with cardiac hypertrophy.
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PMID:Abnormalities in the coronary circulation that occur as a consequence of cardiac hypertrophy. 622 97

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35

During acute myocardial infarction an increase in arterial pressure is common in patients who were previously normotensive and, therefore, do not have left ventricular hypertrophy. However, the effect of hypertension on infarct size in the absence of hypertrophy is uncertain. Thus, 32 open chest dogs underwent a 2 hour occlusion of the mid-left anterior descending coronary artery followed by 3 hours of reperfusion. Immediately after occlusion, 14 dogs were randomized to a hypertension group (intravenous phenylephrine infusion starting 5 minutes after occlusion and terminating at the time of reperfusion, with heart rate kept constant by atrial pacing) and 18 dogs to a control group (equivalent volumes of saline solution intravenously). Twelve of the 32 dogs were excluded from analysis because they developed ventricular fibrillation during coronary occlusion or reperfusion. In the hypertension group (n = 10), the mean arterial pressure increased significantly within 10 minutes of coronary occlusion (146 +/- 7 versus 109 +/- 11 mm Hg in 10 control dogs, p less than 0.01) and was maintained approximately 40 mm Hg higher than in the control group (p less than 0.01) throughout the ischemic period. Heart rate was similar in the two groups throughout the experiment. After the dogs were sacrificed, the region normally supplied by the occluded artery (anatomic "region at risk") was identified by simultaneous perfusion of the aortic root and the coronary artery distal to the occlusion. The heart was sectioned transversely and stained with triphenyltetrazolium-chloride. The infarcted area and the anatomic risk area were determined by video planimetry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of acute arterial hypertension on myocardial infarct size in dogs without left ventricular hypertrophy. 623 49

The effectiveness of dietary changes as a means of reducing blood lipid levels and ultimately controlling the development of coronary heart disease has been debated for many years. The possible effects of alcohol consumption on blood lipids were usually not considered. Our findings indicate a significant positive correlation between the extent of coronary artery occlusion and total plasma cholesterol levels and a negative association between the coronary occlusion and high density lipoprotein (HDL) cholesterol. Since moderate alcohol consumption increases the HDL cholesterol levels, one can also postulate that it affects coronary artery lesions. The attenuating effect of alcohol on the coronary occlusion was negated by sporadic drinking of large amounts of alcohol. In evaluating the possible effect of alcohol on coronary artery disease, it is also necessary to consider its addictive potential as well as other untoward sequelae of alcohol consumption such as hypertension, damage to the myocardium, and increased prevalence of malignancies.
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PMID:Alcohol consumption and the diet-heart controversy. 634 45

Based on data from the literature and their own experience, the authors study the long-term clinical course of patients with interatrial communications (IAC), coarctation of the aorta (CAo) and tetralogy of Fallot (TF) who have been operated. According to data from the literature and 50 cases which were reviewed an average of 11 years after the operation, operated cases of IAC are at risk of developing arrhythmias or conduction disturbances, especially if the operation was performed after the age of 20, in cases with cardiomegaly, with a mean pulmonary artery pressure of more than 20 mmHg and a pulmonary flow/systemic flow ratio due to the shunt greater than 1.5. Surgery for CAo carries a risk of long-term residual hypertension (HT). According to the majority of authors and a study of 55 cases. HT is present in 3 to 6% of cases operated between the ages of 1 and 10 years. This percentage is much higher for the older age groups. The increase in blood pressure on effort and the demonstration of a gradient between the upper limb and the lower limb are the methods of detecting post-operative hypertension and residual stenosis. Cardiac failure and coronary occlusion can occur in the cases which were operated late. Following complete correction of TF, severe ventricular arrhythmias can arise in the long term. From a study of 59 patients at least 3 years after the operation, the authors outline the elements which favour the development of these arrhythmias. The cases at highest risk are those which were operated after the age of 2 years with significant residual lesions, cardiomegaly and ventricular extrasystoles on the resting trace.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term follow up of surgically-treated congenital heart disease: interauricular communication, aortic coarctation, tetralogy of Fallot]. 642 Dec 21

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

Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. Eighty-two dogs instrumented with three to six pairs of pulse-transit piezoelectric crystals were studied in an awake, unsedated state to measure segmental wall thickness. A pneumatic balloon occluder was positioned around the proximal left anterior descending artery (LAD). Thirty-three dogs underwent LAD occlusion and served as normotensive controls (group A). Group B dogs (n = 23) received a 6-hour infusion of phenylephrine (PE) beginning 5 minutes after LAD occlusion to increase aortic diastolic arterial pressure to 120-130 mm Hg; aortic pressure was then allowed to return to normal for the subsequent 18 hours. The eight dogs in group C received a 6-hour infusion of PE, but no coronary arterial occlusion was produced. In group D (n = 12), distal constriction of the thoracic aorta was maintained for 24 hours after LAD occlusion. Regional myocardial blood flow (RMBF) was measured with radioactive microspheres in six conscious dogs and both RMBF and intramyocardial PCO2 were measured in seven open-chest dogs to assess alterations in regional myocardial oxygen supply and demand. Segments of myocardium were arbitrarily grouped according to the amount of net systolic thickening (NET) present 5 minutes after LAD occlusion and before increasing aortic pressure: group 1 retained 67-100+% of control NET, group 2 0-67%, and group 3 less than 0% (paradoxic motion). In dogs receiving PE plus LAD occlusion and in dogs with aortic constriction and LAD occlusion, NET was transiently depressed in groups 1 and 2 compared with the normotensive cohort; 24 hours after occlusion, NET in groups 1, 2 and 3 did not differ significantly from that in the normotensive dogs. Systemic hypertension resulted in a significant increase in endocardial and midwall RMBF and, in seven open-chest dogs, decreased the intramyocardial accumulation of carbon dioxide after LAD occlusion. Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.
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PMID:Effects of systemic hypertension on ischemic and nonischemic regional left ventricular function in awake, unsedated dogs after experimental coronary occlusion. 679 86


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