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

The authors performed a prospective study to correlate echocardiographic left ventricular hypertrophy (LVH) and silent ischemia (SI) detected by twenty-four-hour ambulatory electrocardiographic monitoring with new cardiac events in 355 patients, mean age eighty-two +/- eight years, with systemic hypertension or coronary artery disease (CAD). Cardiac events included myocardial infarction, primary ventricular fibrillation, or sudden cardiac death. Mean follow-up was thirty-one +/- seven months (range twelve to forty). Cardiac events occurred in 28 of 147 patients (19%) without LVH or SI (A), in 56 of 113 patients (50%) with LVH and no SI (B), in 16 of 29 patients (55%) with SI and no LVH (C), and in 52 of 66 patients (79%) with LVH and SI (D). Significant p values were p less than 0.001 comparing D with A, D with B, C with A, and B with A; and p less than 0.02 comparing D with C. These data indicate that echocardiographic LVH and SI detected by ambulatory electrocardiographic monitoring are independent risk factors for new cardiac events in elderly patients with systemic hypertension or CAD.
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PMID:Usefulness of echocardiographic left ventricular hypertrophy and silent ischemia in predicting new cardiac events in elderly patients with systemic hypertension or coronary artery disease. 213 98

Left ventricular hypertrophy caused by cardiovascular disease is a marker as well as a contributing factor for cardiovascular morbidity and mortality. Ventricular tachycardia, complex ventricular arrhythmias, and silent ischemia are more prevalent in patients with left ventricular hypertrophy than in those without. Echocardiography is more sensitive and more specific than electrocardiography in diagnosing the entity. Treatment of the underlying disorder may cause regression of left ventricular hypertrophy which, Framingham Heart Study data suggests, may reduce the incidence of cardiovascular events.
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PMID:Left ventricular hypertrophy. Significance in cardiac morbidity and mortality. 213 88

Tolerance of the canine heart to prolonged ischemic arrest was studied in 10 hearts from normal control dogs and 15 hearts from dogs with left ventricular hypertrophy (LVH); experiments were performed 1 year after banding the aorta in 8-week-old puppies. At 1 year, hemodynamic studies revealed decreased left ventricular (LV) fiber shortening and elevated end-diastolic pressure (EDP) in five dogs (group with LVH failure); 10 dogs exhibited normal shortening and normal EDP (group with LVH compensation). The left ventricle-to-body weight ratio (g/kg) was 4.4 +/- 0.8 in the control group of dogs, 7.7 +/- 1.0 in the group with LVH compensation, and 10 +/- 2.5 in the group with LVH failure. The tolerance to 60 minutes of global ischemia (37 degrees C) followed by 90 minutes of reperfusion was studied in an isolated blood-perfused heart apparatus (isovolumic left ventricle, coronary perfusion pressure of 100 mm Hg). In the baseline (preischemic) state, coronary blood flow, myocardial oxygen consumption, lactate extraction, and myocardial high-energy phosphate content were essentially equal in the three groups; with LV volume adjusted to produce a systolic pressure of 100 mm Hg, there were no significant differences in LVEDP among the three groups. During ischemia, the diastolic (asystolic) pressure increased from 11 +/- 3 to 28 +/- 16 mm Hg (p less than 0.05) in the group with LVH failure; however, it did not increase in the control or the LVH compensation groups. Myocardial ATP levels declined equally in all three groups. During early reperfusion, lactate washout was lowest in the group with LVH failure. By 90 minutes of reperfusion, there were no significant differences in coronary blood flow, myocardial oxygen consumption, lactate extraction, or high-energy phosphate levels. High diastolic pressure persisted at 90 minutes of reperfusion in the LVH failure group (EDP was 34 +/- 19 mm Hg); however, there was no significant change in EDP during reperfusion in the control or with LVH compensation groups. After 90 minutes of reperfusion, developed pressures in the control (54 +/- 9 mm Hg), the LVH compensation (49 +/- 18 mm Hg), and the LVH failure (67 +/- 17 mm Hg) groups were not significantly different. These data indicate that hearts with compensated LVH do not exhibit an impaired tolerance to ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy. 213 93

Balloon dilatation was used to explore the strength of the left ventricular wall in rats. The rupture pressure of the left ventricle was 645 +/- 22 mm Hg and that of the right ventricle was 247 +/- 15 mm Hg in intact animals. Left ventricular hypertrophy induced by 50% ascending aortic stenosis increased rupture pressure proportionally to the degree of hypertrophy. In transmural myocardial infarction occupying 40-55% of the left ventricular wall volume, the rupture pressure within 10 days of myocardial infarction was the same as that in the intact myocardium. Following 24 hours of ischemia, myocardial reperfusion produced no effects, but after 2 or 4 hours of ischemia it reduced the strength of the heart wall by 50%. It was concluded that early thrombolytic therapy might be a risk factor for cardiac rupture in myocardial infarction.
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PMID:[The role of myocardial reperfusion and hypertrophy in the development of heart rupture in experimental myocardial infarction]. 213 4

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

Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.
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PMID:Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy. 214 98

Chronic ventricular hypertrophy caused by pressure overload is a common associated risk factor in congenital cardiac surgery. Because calcium controls contractile protein interaction, we postulated that inducing ventricular hypertrophy from birth alters the way myocytes are able to regulate free cytosolic calcium (Cai) during ischemia. In this study we measured Cai with a recently developed intracellular fluorescent probe trapped inside myocytes by deesterification. The probe shifts its fluorescence spectra (from 380 to 340 nm; fluorescence measured at 510 nm) when it binds to calcium in direct relation to Cai. We studied the effects of ischemia at 37 degrees C (up to 50 minutes) on Cai in newborn (3 to 5 days), adult control (2 to 4 months old), and hypertrophied (2 months old; aortic banding done at 10 days) isolated retroperfused rabbit hearts loaded with Fura-2. In a separate group of hearts (n = 6 per group) we measured isovolumic peak developed pressure with an intracavity balloon in hearts subjected to 30 minutes of ischemia at 37 degrees C and 30 minutes of reperfusion. The recovery of peak developed pressure (percent of preischemic control) was 101% +/- 6% in control, 85% +/- 4% (p less than 0.05 vs control) in newborn, and 67% +/- 7% (p less than 0.05 vs control) in hypertrophied hearts. Cai-dependent fluorescence rose to 160% +/- 30% of preischemic baseline levels by 30 minutes of ischemia in control versus a decline to 55% +/- 7% (p less than 0.05 vs control) in newborn and 51% +/- 2% (p less than 0.05 vs control) in hypertrophied hearts by 30 minutes of ischemia. We conclude that hypertrophied and newborn hearts have a lower Cai during ischemia compared with adult hearts, and this is associated with a worse recovery of cardiac function. The lower Cai may be the result of irreversible binding of calcium to contractile proteins.
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PMID:The effect of cardiac hypertrophy on changes in cytosolic free calcium concentration during ischemia. 214 18

Eighteen dogs underwent transmural left ventricular biopsies for adenosine triphosphate and suturing of the noncoronary cusp, creating valvular aortic stenosis. Three months after aortic stenosis and the subsequent development of left ventricular hypertrophy, animals underwent repeat transmural left ventricular biopsies followed by total myocardial ischemia at 37 degrees C. Left ventricular tissue samples for adenosine triphosphate and lactate levels were determined at 15-minute intervals and compared with 15 control animals. No significant difference between subendocardial and subepicardial adenosine triphosphate levels was found between left ventricular samples taken before left ventricular hypertrophy and 3 months after left ventricular hypertrophy. Significant differences in adenosine triphosphate utilization occurred between subendocardial and subepicardial layers in control and left ventricular hypertrophy myocardium, however. The gradient between the subendocardium and the subepicardium was significantly increased by left ventricular hypertrophy (p less than 0.05). Significant differences also occurred within the same layer when left ventricular hypertrophy and control groups were compared. During total ischemia, lactate concentration was significantly greater within the subendocardium than within the subepicardium in left ventricular hypertrophy. The onset of ischemic contracture was 48.2 +/- 2.1 minutes in left ventricular hypertrophy versus 62.3 +/- 1.8 minutes in control hearts (p less than 0.01). Subendocardial intramyocardial pressure increased significantly earlier than subepicardial in both left ventricular hypertrophy and control hearts. Adenosine triphosphate was used, and lactate accumulated more rapidly in animals with a more pronounced hemodynamic gradient. These data show that after left ventricular hypertrophy, adenosine triphosphate stores in the subendocardium and the subepicardium are unchanged from control values, yet the rates of adenosine triphosphate utilization and lactate accumulation during total ischemia are significantly increased. Furthermore, the subendocardial to subepicardial gradient of adenosine triphosphate utilization during ischemia found in normal hearts is markedly increased by left ventricular hypertrophy.
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PMID:Accelerated transmural gradients of energy compound metabolism resulting from left ventricular hypertrophy. 214 78

ECG evidence of silent ischemia occurs commonly in patients with systemic hypertension, but its relationship to left ventricular hypertrophy (LVH), large-vessel coronary artery disease (CAD), and neurohumoral factors remains unclear. Accordingly we validated the results of the echocardiographic method used to measure left ventricular (LV) mass in the Soviet Union by comparison with necropsy measurements in 30 patients, and we examined the relationships in 46 men with essential hypertension among ST segment depression during ambulatory monitoring, exercise stress and transesophageal pacing (n = 38), and LV mass, catheterization evidence of CAD (n = 25), and neurohumoral factors (plasma catecholamines and platelet aggregability). Echocardiographic measurements of LV mass by both the Soviet and Penn methods were closely correlated with necropsy values (r = 0.78 and 90, respectively; both p less than 0.001). During ambulatory monitoring from 1 to 17 episodes of greater than or equal to 1 mm ST depression occurred in 26 of 46 (65%) patients with hypertension; ischemia was also provoked by exercise or pacing stress in most but not all of these patients (65% and 80%, respectively). Neither ST depression nor the occurrence of additional episodes of symptomatic angina was related to the presence of coronary obstruction at catheterization; patients with and without ST depression did not differ in age, blood pressure, or LV mass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive heart disease: relationship of silent ischemia to coronary artery disease and left ventricular hypertrophy. 214 35

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.
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PMID:Progress in cardioprotection: the role of calcium antagonists. 214 58


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