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)

Recognition and diagnosis of nonobstructive apical hypertrophic cardiomyopathy is important to begin to understand the natural history and prognosis of such patients. Our experience with three patients indicates that a clue to the recognition of apical hypertrophic cardiomyopathy lies in the striking electrocardiographic repolarization changes consistent with subendocardial ischemia often prompting admission to the coronary care unit. The diagnosis of apical hypertrophic cardiomyopathy in two patients was confirmed by two-dimensional echocardiographic apical views, but due to a technically inadequate echocardiogram, the diagnosis in the third patient was made by left ventriculography. Two of the three patients underwent right and left cardiac catheterization and their rest and exercise hemodynamic data were consistent with restrictive cardiomyopathy.
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PMID:Recognition and diagnosis of apical hypertrophic cardiomyopathy. 668 14

The calcium channel blocking agents have multiple hemodynamic effects that make them potentially valuable in treating many cardiovascular disorders. They are potent dilators of coronary and peripheral arteries and in isolated tissue preparations exert potent negative inotropic, chronotropic, and dromotropic effects. In intact animals the peripheral arterial vasodilatation induces reflex-mediated adrenergic activity, which opposes the direct negative inotropic, chronotropic, dromotropic, and hypotensive effects. The individual calcium channel blockers have different relative potencies on various cardiovascular functions. The net hemodynamic and electrophysiologic effect of each agent, therefore, results from a complex interplay of direct and reflex phenomena. The clinical efficacy of these agents in classic angina pectoris relates to their ability to decrease afterload, myocardial contractility, and heart rate and increase coronary blood flow. The agents have been used to prevent coronary spasm in Prinzmetal's variant angina. The negative inotropic effects of verapamil are valuable in improving the symptoms and hemodynamic disturbances of hypertrophic cardiomyopathy. The role of these agents in treating arterial hypertension, unstable angina pectoris, acute myocardial infarction, and ischemia during cardiopulmonary bypass needs to be determined.
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PMID:Calcium channel blocking agents in the treatment of cardiovascular disorders. Part II: Hemodynamic effects and clinical applications. 700 93

To clarify the pathogenesis of chest pain in patients with cardiomyopathies, we compared coronary blood flow and other indicators of ischemia at rest and during pacing-induced tachycardia in nine patients with cardiomyopathy (four hypertrophic and five congestive) and in five control subjects. Coronary blood flow was reduced at rest and during pacing in cardiomyopathy patients compared with controls. In patients with hypertrophic cardiomyopathy, pacing induced chest pain in all, increased ST-segment depression in three patients and increased coronary venous lactate concentration. With pacing, two of five patients with congestive cardiomyopathy had chest discomfort and three had increased ST-segment depression, but coronary venous lactate concentration did not change significantly. In both groups of cardiomyopathies, the ratio of the systolic and diastolic pressure-time indexes tended to decrease more than in controls during pacing. Thus, myocardial perfusion is decreased in patients with cardiomyopathy, both at rest and during pacing. The changes detected during pacing point to subendocardial ischemia as the likely mechanism for angina in hypertrophic and possibly also in congestive cardiomyopathy.
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PMID:Pathophysiology of chest pain in patients with cardiomyopathies and normal coronary arteries. 719 3

We report the pathologic changes of the cardiac conduction tissue (CS) in 33 cases of sudden cardiac death. The cases were divided into two groups: those with severe atherosclerotic coronary lesion (> 75% cross-sectional area stenosis of at least one coronary artery), 15 cases, and those without significant coronary disease, 18 cases. In the first group, we observed major changes of the CS in eight cases. The changes consisted of abnormalities in His bundle position (branching bundle in pars membranacea or left-sided bundle), atrioventricular (AV) node fibrosis, and interatrial lipoma. Other age-related minor abnormalities such as mild fibrosis, fatty change, or fibrointimal hyperplasia of CS arteries were observed in nine cases. In the second group, major lesions of the CS were recognized in 13 cases: abnormalities in bundle branch position in eight cases (left-sided, inside the membranous septum), downward displacement of the tricuspid valve with AV node elongation in three cases, and a single case with one of the following: His compression by hypertrophic cardiomyopathy, Mahaim fibers, focal ischemia of bundle, AV node division, AV node dissection by edema, intramural left bundle branch, or tumor of the AV node. In the study of the pathogenesis of sudden death, the conduction system lesions always have to be considered, even in cases with severe coronary disease.
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PMID:Pathologic changes of the cardiac conduction tissue in sudden cardiac death. 749 58

Various evidence suggest that myocardial ischemia is a major factor in the progression of hypertrophic cardiomyopathy (HCM). In this study, we investigated the effects of nicorandil on left ventricular (LV) systolic and diastolic function in 12 symptomatic patients with HCM using echocardiography and radionuclide angiography. Nicorandil (6 mg), when administered intravenously, produced no significant changes in any parameter, including LV filling dynamics. However, accelerated LV peak early filling velocity (0.51 +/- 0.13 to 0.59 +/- 0.14 m/sec, p < 0.01), and reduced peak velocity in atrial contraction (0.54 +/- 0.17 to 0.50 +/- 0.15 m/sec, p < 0.05) were observed by Doppler echocardiography after 4 weeks of oral administration of 10 mg nicorandil 3 times daily. This oral administration did not affect heart rate, blood pressure, LV outflow gradient, or LV systolic function. The same favorable results were observed in a wall motion analysis with radionuclide angiography: peak filling rate (PFR) in global LV (3.21 +/- 0.76 to 3.52 +/- 0.87 end-diastolic volume (EDV)/sec, p < 0.02), and apical (4.73 +/- 1.18 to 5.42 +/- 1.55 EDV/sec, p < 0.01) and lateral (4.78 +/- 1.60 to 5.52 +/- 1.51 EDV/sec, p < 0.05) segments was increased, and the time to peak filling rate (TPF) in septal (245 +/- 31 to 203 +/- 40 msec, p < 0.01) and lateral (222 +/- 54 to 193 +/- 34 msec, p < 0.05) segments was reduced. These findings indicate that nicorandil has beneficial effects on LV diastolic function in HCM. These favorable effects may be due to the improvement of subendocardial ischemia.
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PMID:Effects of nicorandil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy. 760 50

Despite recent evidence that angiotensin-converting enzyme (ACE) inhibitors reduce mortality in patients with congestive heart failure (CHF), it is important to note that roughly 40% of patients with New York Heart Association class I-III disease treated with these agents died during 4-year follow-up in the treatment arm of two large trials. Given this high mortality rate, there is an obvious need for therapy beyond digoxin, diuretics, and ACE inhibitors. Digoxin is associated with favorable effects on exercise capacity, ejection fraction, and clinical symptomatology in the majority of patients with CHF. Its effects on mortality are unknown, but are the subject of a continuing trial sponsored by the National Institutes of Health. The beta-agonists are also associated with hemodynamic and clinical improvements in patients with CHF, but probably increase the risk of mortality, especially when taken on a long-term basis. Therefore, their use should be limited to the short-term management of acute exacerbations of CHF. Phosphodiesterase inhibitors, particularly milrinone, are associated with increased mortality in patients with CHF, apparently related to their arrhythmogenic effect. Little evidence exists that calcium channel blockers exert beneficial effects in patients with CHF (unlike their role in hypertrophic cardiomyopathy); indeed, first-generation calcium channel blockers may be detrimental in patients with left ventricular dysfunction and they should generally be avoided in this setting. Treatment of ischemia in patients with CHF should be initiated with nitrates; low dosages of vasoselective dihydropyridine calcium channel blockers may be attempted if nitrates fail.
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PMID:Assessing the treatment of congestive heart failure: inotropic agents and calcium channel blockers. 790 42

Eight hearts with pulmonary atresia with intact ventricular septum were studied grossly and microscopically. The right ventricle was composed of inlet, infundibular, and trabecular portions in two hearts, without trabecular portions in three hearts, and consisted of an inlet part only in another three hearts. Pulmonary atresia was classified as membranous in two hearts; the other six hearts had muscular atresia. The left ventricle showed a range of abnormalities, albeit mostly discrete. A mitral valve with short tendinous chords was present in four hearts; one of these had a cleft mitral valve. All hearts (except the heart of a 1-day-old neonate) had a prominent subaortic septal bulge. All hearts had left ventricular hypertrophy, which exceeded twice the standard deviation of normal in two patients. None of the hearts had histologic features of hypertrophic cardiomyopathy. The density of intramyocardial coronary arteries was normal in each patient, but medial thickening (20 to 100 microns diameter arteries) had occurred in four patients. Signs of acute myocardial ischemia (hydropic cell swelling) were present in all; one heart (the oldest case of 6 months) contained areas of replacement fibrosis and calcifications indicative of previous infarction. Quantification of the volume density of endomysial (interfiber) collagen (Picrosirius red microspectrophotometry) showed high levels in all, within the range of normal in five patients, but exceeding twice the standard deviation of normal in three patients. In all cases the values obtained in the subendocardial layers were higher than those obtained subepicardially. The observations show that the left ventricle in hearts with pulmonary atresia with intact ventricular septum contains abnormalities that may render the left ventricle less capable to cope with a volume load. The high values of endomysial (interfiber) collagen suggest chronic ischemia in relation to left ventricular hypertrophy as the main mechanism involved. Therefore, as a late consequence, the left ventricle could be the limiting factor for long-lasting successful surgical intervention.
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PMID:Disease of the left ventricle in pulmonary atresia with intact ventricular septum. The limiting factor for long-lasting successful surgical intervention? 802 53

Previous invasive studies have suggested that coronary flow reserve is impaired in patients with left ventricular hypertrophy (LVH) and symptoms of ischemia. We tested whether transesophageal Doppler, a semiinvasive technique, can detect altered characteristics of baseline coronary blood flow velocity in such patients. Thirty patients with LVH (hypertrophic cardiomyopathy in 4, aortic stenosis in 17, hypertension in 9) were studied. Fourteen patients had asymptomatic LVH. Sixteen patients had clinical symptoms of ischemia with angiographically normal epicardial coronary arteries. Ten subjects with no cardiovascular disease were studied as a control group. Peak diastolic and systolic coronary flow velocities were recorded in the proximal part of the left anterior descending artery (LAD) with the use of pulsed Doppler guided by color flow imaging. Patients with symptomatic LVH had higher diastolic peak coronary flow velocity (81 +/- 10 cm/sec, p = 0.0001) compared with normal subjects (41 +/- 8 cm/sec) and patients with asymptomatic LVH (44 +/- 8 cm/sec). In patients with asymptomatic LVH the diastolic coronary flow velocity/indexed ventricular mass ratio was lower (0.28 +/- 0.09 cm/gm/m2, p = 0.0001) compared with symptomatic patients (0.52 +/- 0.12 cm/gm/m2) and compared with controls (0.47 +/- 0.16 cm/gm/m2). Patients with symptomatic LVH but no aortic stenosis also had higher peak systolic coronary flow velocity (38 +/- 9 cm/sec) compared with the other groups (p = 0.0001). In the group of patients with aortic stenosis a significant inverse linear relation was found between peak systolic coronary flow velocity and peak pressure gradient (r = -0.60, p 0.01). In conclusion, patients with symptomatic LVH have abnormally high baseline coronary flow velocities resulting in magnified intimal shear stress. Because flow velocity equals flow/vessel cross-sectional area, it is suggested that high coronary flow velocities in patients with symptomatic LVH result from both augmented coronary flow and failure of the vessel to enlarge commensurately with the increase in LV mass (relative functional stenosis). In patients with aortic stenosis, peak systolic coronary flow velocity appears to be influenced by transvalvular pressure drop.
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PMID:Abnormal coronary flow velocity pattern in patients with left ventricular hypertrophy, angina pectoris, and normal coronary arteries: a transesophageal Doppler echocardiographic study. 807 11

The effect of verapamil on myocardial ischemia in patients with hypertrophic cardiomyopathy (HCM) was evaluated by exercise myocardial 201Tl SPECT (EX-Tl). EX-Tl was performed before and after 8.1 +/- 6.1 weeks of oral administration of verapamil (240 mg/day) on 20 patients with HCM who showed transient 201Tl perfusion defects under control conditions. SPECT images were divided into nine segments. The 201Tl perfusion defect was visually scored and evaluated for four grades in each segment and the sum total grade was calculated as the defect score. Transient dilation index was calculated as a reflection of subendocardial ischemia. Improvements in defect score were demonstrated in 18 of 20 patients after administration of verapamil. The mean defect score decreased significantly from 5.1 +/- 2.3 to 2.5 +/- 2.4 (p < 0.001). Although 18 of 20 patients showed abnormal transient dilation index under control conditions, 16 showed improvement and 12 were normalized after verapamil therapy. Mean transient dilation index decreased from 1.24 +/- 0.19 to 1.08 +/- 0.10 (p < 0.01). Verapamil improves myocardial ischemia in patients with HCM.
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PMID:[Effect of verapamil on myocardial ischemia in patients with hypertrophic cardiomyopathy: evaluation by exercise thallium-201 SPECT]. 815 30

Myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM) may play an important role in the function and/or dimensions of the left ventricle. We present an autopsied case of HCM followed for 10 years. A 68-year-woman with HCM underwent trans-aortic myectomy of the interventricular septum in 1979. A significant amount of round cell infiltration, myocardial fibrosis and disarray were observed in the resected specimen. She experienced repeated admissions due to diabetes mellitus and congestive heart failure, and died of renal failure in 1989. An autopsy revealed extensive myocardial fibrosis and significant cell infiltration in the ventricular myocardium. The infiltrating cells were almost all lymphocytes, and the ratio of CD4 to CD8 was 3.8. This ratio was different from that of typical viral myocarditis. This case suggests that there may be an undefined inflammatory process causing fibrosis in HCM, in addition to the ischemia due to intramural small coronary artery stenosis.
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PMID:An autopsy case of hypertrophic cardiomyopathy with pathological findings suggesting chronic myocarditis. 820 86


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