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)

An increase in left ventricular diastolic pressure has been repeatedly observed during angina in patients with coronary artery stenoses and regional demand ischemia, but the role of relaxation abnormalities versus left ventricular segmental dyssynchrony is controversial. In contrast, patients with angina due to aortic stenosis are likely to have diffuse rather than segmental ischemia and thus may provide an alternative model for examining the diastolic physiology of angina in man. Accordingly, we examined the hemodynamic manifestations of angina in eight patients with aortic stenosis without significant coronary artery disease. Angina was induced by pacing tachycardia, and hemodynamic and echocardiographic variables were measured in the control period and during angina in the beats immediately after cessation of pacing. Heart rate (control vs angina, 69 +/- 12 vs 70 +/- 11 beats/min, p = NS) and left ventricular peak systolic pressure (207 +/- 39 vs 222 +/- 22 mm Hg, p = NS) were similar in the control and postpacing angina periods. Left ventricular end-diastolic pressure, on the other hand, was significantly higher during postpacing angina (15 +/- 7 vs 28 +/- 8 mm Hg, p less than .01). The time constant of left ventricular pressure decline during isovolumetric relaxation (TL), calculated as the slope of a linear fit of the natural log of pressure vs time, increased from 44 +/- 5 to 51 +/- 7 msec (p less than .05); the time constant TD, derived from the slope of a linear fit of dP/dt vs pressure, also increased slightly, although the change was not statistically significant (69 +/- 5 vs 75 +/- 5 msec, p = .06).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered left ventricular diastolic properties during pacing-induced angina in patients with aortic stenosis. 375 81

Valvar aortic stenosis can result in myocardial underperfusion with or without coronary obstruction. The purpose of this study was to determine how hearts with valvar aortic stenosis without hypertrophy can maintain their oxygen supply/consumption balance with partial left anterior descending coronary artery (LAD) occlusion. Open-chested, anesthetized dogs (n = 9) were subjected to mild valvar aortic stenosis and then to a reduction of LAD flow to 50% of baseline, while controls (n = 9) received partial LAD occlusion without aortic stenosis. Blood flows were determined before and after aortic stenosis and after LAD occlusion using radioactive microspheres. The hearts were then removed for microspectrophotometric analysis of regional venous and arterial oxygen saturation. Aortic stenosis resulted in a pressure gradient of approximately 50 mm Hg, representing mild aortic stenosis. Only a slight increase in myocardial blood flow was seen with aortic stenosis. Ischemia resulted in a significant drop in blood flow in control (40%) and aortic stenosis (55%) animals compared with their own preocclusion values. These ischemic region flows were not different from each other. Aortic stenosis itself did not alter oxygen extraction, although partial occlusion similarly increased extraction for all groups in the ischemic zone. The LAD occlusion resulted in a decreased oxygen consumption in the occluded region of all groups, with no differences noted between control and aortic stenosed animals. Thus, mild, acute aortic stenosis without hypertrophy does not appear to significantly increase the severity of an ischemic episode precipitated by partial LAD occlusion.
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PMID:Effect of aortic stenosis on oxygen balance in partially ischemic myocardium. 382 69

Intraaortic balloon counterpulsation was instituted in two adult patients whose condition was rapidly deteriorating because of critical decompensated valvular aortic stenosis. The acute hemodynamic effect of counterpulsation in these patients was compared with the effect of counterpulsation in three control patients with unstable angina and no aortic valve disease. Augmentation of aortic diastolic pressure was similar in both groups; however, in contrast to the patients with unstable angina, the patients with aortic stenosis had no decrease in left ventricular systolic pressure. Counterpulsation resulted in an increase in the transvalvular pressure gradient, which was associated with a slight increase in stroke volume. In both patients with aortic stenosis, the institution of counterpulsation resulted in marked clinical improvement, which facilitated successful valve replacement surgery. The benefit from counterpulsation in critically decompensated aortic stenosis appears to be derived almost entirely from augmentation of the diastolic coronary filling gradient. The improvement that results from counterpulsation suggests that ischemia is the major cause of decompensation.
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PMID:Intraaortic balloon counterpulsation as a temporary support measure in decompensated critical aortic stenosis. 397 70

Stereological techniques were used to determine quantitatively the changes in subcellular organelles in the hypertrophied swine heart. Hypertrophy was induced by aortic stenosis. In addition, the animals were stressed by exercising twice weekly on the treadmill for 30 days. The controls were normal animals which were neither exercised nor had aortic stenosis. Tissue samples from the left ventricle and interventricular septum were processed for electron microscopy. Relative volumes of myofibrils, mitochondria, transverse tubular system (T-system) sarcoplasmic reticulum (SR), and clear intracellular space (ICS) were measured. Significant differences in the volumes of all the components except the T-system were found between experimental and control animals in the epicardial and endocardial regions of the left ventricle and interventricular septum. Mitochondria and myofibrils were significantly decreased in the exercise stressed hypertrophied hearts as reported in ischemia, while SR and ICS were significantly increased. These findings suggest that ischemic injury occurs in all regions of the hypertrophied heart wall subjected to acute exercise stress, not solely the endocardial region as previous qualitative studies suggested.
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PMID:Effect of acute exercise stress in cardiac hypertrophy. II. Quantitative ultrastructural changes in the myocardial cell. 612 35

It is frequently stated that hypertrophied ventricles tolerate ischemia less well than nonhypertrophied ventricles. The authors' earlier studies in a rat supravalvular aortic stenosis model and canine valvular aortic stenosis model, both with concentric left ventricular hypertrophy, disclosed accelerated rates of ischemic contracture and diminished basal myocardial high energy phosphate stores. These studies have been extended to ten patients with severe left ventricular hypertrophy caused by valvular aortic stenosis and normal coronary arteries. ATP (endocardial and epicardial) from transmural left ventricular biopsies taken at operation before aorta cross-clamping, and frozen immediately in liquid nitrogen, were compared with similar biopsies from patients with nonhypertrophied myocardium supplied by normal coronary arteries. The subendocardial high energy phosphate levels in the nonhypertrophied myocardium was greater than high energy phosphate levels in the subepicardium of nonhypertrophied ventricles (ATP-micromoles/gram-protein, epi = 36.8 +/- 3.3, endo = 37.7 +/- 3.3) (p = NS). However, in the hypertrophied myocardium the subendocardium consistently showed significantly depressed high-energy phosphate levels when compared with subepicardial levels (ATP-hypertrophied myocardium, epi = 31.5 +/- 1.6, endo = 25.9 +/- 1.7) (p less than 0.05). This uniform depression of ATP stores, greatest in the subendocardium, in left ventricular hypertrophy suggests a common biologic mechanism for the enhanced sensitivity to ischemia. Of importance for patients may be the prior observation in rats that repletion of ATP( stores before ischemia eliminates the accelerated rate to ischemic contracture. Diminished subendocardial ATP stores appear to be an intrinsic property of severely hypertrophied myocardium and probably contribute to its enhanced sensitivity to ischemia.
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PMID:Depressed high-energy phosphate content in hypertrophied ventricles of animal and man: the biologic basis for increased sensitivity to ischemic injury. 621 20

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

The effect of hypothermic ischemic arrest on myocardial contractility was investigated with use of isolated blood-perfused canine heart preparation in the hypertrophied left ventricle created by supravascular aortic stenosis and the non-hypertrophied ventricle. The following results were obtained: The percent recovery rate of net developed tension during reperfusion after an ischemic period of 150 minutes at the myocardial temperature of 17 degrees C was 90 +/- 9% in the non-hypertrophied muscle, that is, hypertrophied left ventricle was considered to be more vulnerable to ischemia as compared to nonhypertrophied left ventricle, suggesting the necessity of more intense myocardial protection in addition to cardiac hypothermia against ischemia in the hypertrophied heart.
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PMID:Effect of hypothermia during ischemia on myocardial contractility in nonhypertrophied and hypertrophied ventricles. 624 89

Cardiac receptors include both mechanically and chemically sensitive receptors located in atria and in ventricles. Atrial receptors innervated by myelinated vagal afferent fibers reflexly regulate heart rate and intravascular volume. On the other hand, stimulation of ventricular receptors can cause either reflex bradycardia and hypotension or, alternatively, excitation of the cardiovascular system. The former response is mediated by vagal afferents, whereas the latter is mediated by sympathetic (spinal) afferents. Under normal circumstances, cardiac receptors sense changes in wall motion or diastolic pressure and perhaps provide a fine tuning of the cardiovascular system. However, under certain pathological conditions such as coronary ischemia, which cause release of substances such as bradykinin and prostaglandins, there is an exaggerated response of the ventricular receptors. Because these receptors cause a reflex depression of the cardiovascular system and, in particular, induce renal vasodilation, they may protect the heart and kidney by lessening myocardial oxygen requirements and by increasing renal blood flow. In the situation of heart failure both atrial and ventricular receptors are reset and therefore provide for an exaggerated neurohumoral discharge. Finally, patients with aortic stenosis may demonstrate a paradoxical vasodilation and syncope during exercise when there likely is excessive stimulation of left ventricular receptors by the high transmural pressure.
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PMID:Cardiac receptors: their function in health and disease. 638 3

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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