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)

Abnormalities of left ventricular (LV) systolic performance develop during exercise in patients with coronary artery disease (CAD) as a result of ischemia-induced regional wall motion abnormalities. Like patients with hypertension and those with hypertrophic cardiomyopathy, patients with CAD display abnormalities of LV diastolic performance under basal conditions in the absence of ischemia. The purpose of these studies was to compare the effects of bepridil versus those of propranolol or diltiazem in patients with exertional angina pectoris. LV systolic and diastolic performance were assessed at rest and during peak upright bicycle exercise by first-pass radionuclide ventriculography. Compared with propranolol, bepridil increased exercise capacity, cardiac output, and stroke volume and decreased systemic vascular resistance. Compared with diltiazem, bepridil increased exercise capacity, peak filling rate, and early diastolic filling fraction and decreased systemic vascular resistance, heart rate, time to peak filling rate, and atrial filling volume. Bepridil therapy is associated with improved exercise capacity and decreased anginal frequency and nitroglycerin consumption. In addition, its use is accompanied by favorable changes in LV systolic and diastolic function at rest and during exercise. These changes are consistent with benefits resulting from resolution of myocardial ischemia as well as from positive lusitropic effects of bepridil on the ventricular myocardium.
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PMID:Effects of antianginal therapy on left ventricular systolic and diastolic performance: comparison of the response to bepridil, propranolol, and diltiazem. 155 88

A sixty-four-year-old man presented with repolarization abnormalities on the electrocardiogram. Echocardiography and cardiac catheterization revealed that he had the rare combination of apical hypertrophic cardiomyopathy with bilateral coronary-artery-to-pulmonary-artery fistula. An exercise thallium scan was negative, suggesting that the marked electrocardiographic changes were most likely secondary to the apical myocardial hypertrophy, instead of to coronary-steal-induced ischemia.
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PMID:Bilateral coronary-artery-to-pulmonary-artery fistula coexistent with apical hypertrophic cardiomyopathy--a case report. 155 56

Myocardial thallium-201 (Tl-201) imaging performed in conjunction with exercise stress has enhanced the accuracy of detecting coronary artery disease among patients with chest pain. Sensitivity and specificity of qualitative visual Tl-201 scintigraphy for detection of coronary artery disease average 84% and 87%, respectively. Quantitative analysis of planar Tl-201 scintigrams has yielded sensitivity and specificity in the 90% range. Single photon emission computed tomographic imaging is associated with even higher sensitivity but with specificity in the 82-85% range. Perfusion defects representing ischemia can now be distinguished from scar by demonstration of delayed Tl-201 redistribution or enhanced uptake after reinjection of a second dose of Tl-201. Stenoses of the left circumflex coronary artery are less easily detected than lesions of the right and left anterior descending coronary arteries. False-positive Tl-201 perfusion defects may occur as a result of attenuation artifacts, most often caused by overlying breast tissue or by a high left hemidiaphragm. Patient motion during acquisition of single photon emission computed tomographic images results in artifactual defects on reconstruction. Abnormal Tl-201 uptake has been noted in patients with 1) left bundle branch block and normal coronary arteries, 2) hypertrophic cardiomyopathy, and 3) progressive systemic sclerosis.
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PMID:Diagnostic accuracy of thallium-201 myocardial perfusion imaging. 188 75

Clinical implications of diffuse slow washout of thallium-201 (DSWO) in exercise-redistribution myocardial SPECT were studied. Thallium-201 washout rate was calculated by Bull's-eye method. DSWO was defined as having abnormal thallium-201 washout rate (less than 30% per 3 hours) in more than two thirds of each coronary artery (CA) area. OF 974 patients whose exercise heart rate exceeded 120/min, 51 (5.2%) showed DSWO and coronary angiography was performed in 43. Twenty-three patients (53%) showed triple vessel disease (3VD), 8 (19%) showed single or double vessel disease (1VD/2VD) and 12 (28%) showed normal CA. Patients with normal CA consisted of 6 patients with hypertrophic cardiomyopathy (HCM), 5 with hypertension (HT) and one with electrocardiographic abnormality only. The causes of DSWO were assessed from the history of effort angina (EA) and congestive heart failure (CHF), delayed fill-in of the perfusion defect and the ratio of lung to heart thallium-201 activity (L/M) at exercise as an indicator of the left ventricular (LV) function. High prevalence of EA (74%), high incidence of scintigraphic delayed fill-in (83%) and normal L/M suggested diffuse LV ischemia as the cause of DSWO in 3VD. On the other hand in patients with 1VD/2VD, LV dysfunction at exercise was considered as the cause of DSWO because of low prevalence of EA (13%) and scintigraphic delayed fill-in (13%) (p less than 0.01, p less than 0.005 each vs 3VD), and high L/M (p less than 0.001 vs 3VD) and high prevalence of CHF (38%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical implications of diffuse slow washout of thallium-201 in exercise stress myocardial SPECT]. 192 Sep 45

Heart muscle perfusion was studied by exertion scintigraphy Tal-201 in 24 patients, 16M and 8F, aged 16-45 years, means--28 +/- 7.4 years with hypertrophic cardiomyopathy. The relationship between perfusion disturbances and sudden death risk factors occurring in this group of patients was evaluated. Disturbances of heart muscle perfusion were found in 20 pts (83%); 2 pts had permanent perfusion defects, in 18 pts these defects were completely or partially reversible at rest. Only 4 pts (17%) had normal heart muscle perfusion. In patients with perfusion disturbances there was found a significantly more frequent occurrence of the following sudden death risk factors: 1. syncope (p less than .01) 2. ventricular arrhythmia of IV b class according to Lown (p less than .01) 3. advanced hypertrophy of intraventricular septum (p less than .01) 4. sudden death in patients families (p less than .05) The evaluation of the heart muscle perfusion confirmed the occurrence of myocardial ischemia in most of the examined patients. Normal coronaro-angiography in all the patients over 35 years as well as the young age of the other patients exclude atherosclerosis as the cause of myocardiac ischemia in the group under study. This is a confirmation of nonatherosclerotic etiology of myocardiac ischemia in hypertrophic cardiomyopathy patients. The correlation between perfusion disturbances and sudden death risk factors points to the role of ischemia in the natural course of disease and the value of exertion scintigraphy TI-201 in prognosing patients with hypertrophic cardiomyopathy.
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PMID:[Disturbances of myocardial perfusion by exertion scintigraphy in patients with hypertrophic cardiomyopathy and their relationship with sudden death risk factors]. 194 60

Impaired diastolic function of the hypertrophied and stiffened left ventricle is a characteristic feature of hypertrophic cardiomyopathy (Figure 1). Altered left ventricular filling dynamics and reduced left ventricular distensibility or increased left ventricular diastolic chamber stiffness are associated with reduced left ventricular stroke volume, increased left ventricular filling pressures and compressive effects on the coronary microcirculation. These factors contribute importantly to the clinical presentation of many patients, including symptoms of fatigue, dyspnea and angina pectoris. Reduced distensibility results both from factors determining the passive elastic properties of the ventricular chamber (including severity of hypertrophy, fibrosis and cellular disarray) and from factors influencing the rate and extent of active left ventricular relaxation (Figure 2). The factors contributing to impaired relaxation in hypertrophic cardiomyopathy are mediated via either inactivation dependent or load-dependent mechanisms. In laboratory animals, compromise of myocardial inactivation results in a persistent increase in intracellular calcium concentration and in prolonged interaction of the contractile proteins. Additionally, there is evidence for an increased number of active receptors for calcium antagonists and, lastly, for myocardial ischemia (Figure 3). Load-dependent mechanisms include diminished wall tension at the opening of the mitral valve, changes in afterload, contractility and coronary flow. Other factors are nonuniform and asynchronous regional ventricular function due to differing increases in thickness of the ventricular walls and ischemia (Figure 4). Calcium channel blockers exert a favorable influence on left ventricular relaxation and filling (Figure 5); verapamil and diltiazem are preferable to nifedipine. Verapamil increases left ventricular stroke volume without an increase in the end-diastolic pressure (Figure 6), reduces regional asynchrony if present, and leads to a more homogeneous regional diastolic filling (Figure 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular diastolic function in hypertrophic cardiomyopathy. 202 81

We present a case of association of apical hypertrophic cardiomyopathy of the Japanese type and coronary arteriovenous fistula in a 56-year-old male who presented with anginal symptoms. Both cardiopathies can produce myocardial ischemia and angina, and their association could aggravate the ischemia. In our patient the symptoms were adequately controlled with Verapamil. The coexistence of these two rare entities in the same patient has recently been described in 2 other cases, allowing us to speculate on a possible etiological relation between the 2 abnormalities, probably both been originated in a common developmental error.
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PMID:[Apical hypertrophic cardiomyopathy and coronary arteriovenous fistula]. 206 59

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

The causes of chest pain in patients found to have angiographically normal coronary arteries during cardiac catheterization remain controversial. Cardiac sensitivity to catheter manipulation, pacing at various stimulus intensities and intracoronary injection of contrast medium was examined in several groups of patients who underwent cardiac catheterization. Right heart (especially right ventricular) catheter manipulation and pacing and intracoronary contrast medium provoked chest pain typical of that previously experienced in 29 (81%) of 36 patients with chest pain and angiographically normal coronary arteries and 15 (46%) of 33 symptomatic patients with hypertrophic cardiomyopathy. In contrast, only 2 (6%) of 33 symptomatic patients with coronary artery disease experienced their typical chest pain with these sensitivity tests (p less than 0.001). None of 10 patients with valvular heart disease but without a chest pain syndrome experienced any sensation with these tests. Cutaneous pain threshold testing demonstrated that patients with chest pain and normal coronary arteries had a higher pain threshold to thermal stimulation compared with patients who had coronary artery disease or hypertrophic cardiomyopathy. No relation existed between cardiac sensitivity and cutaneous sensitivity testing. Thus, patients who have chest pain despite angiographically normal coronary arteries may have abnormal cardiac sensitivity to a variety of stimuli. This increased sensitivity may be of causal importance to their chest pain syndrome or may contribute to their perception of ischemia-induced pain. The same phenomenon was also commonly seen in symptomatic patients with hypertrophic cardiomyopathy. Whether this phenomenon represents abnormal activation of pain receptors within the heart or abnormal processing of visceral afferent neural impulses in the peripheral or central nervous system is unknown.
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PMID:Abnormal cardiac sensitivity in patients with chest pain and normal coronary arteries. 222 87

Previous observations suggest the presence of ischemia in the disproportionately thickened interventricular septum (IVS) of patients with hypertrophic cardiomyopathy (HCM), although the details remain obscure. Utilizing digital subtraction coronary angiography (DSA) with LAO projection before and after intracoronary papaverine (P) injection, we evaluated regional myocardial coronary blood flow reserve (rMFR) consecutively 18 patients with HCM, and compared it with that of 8 patients without apparent cardiac abnormality (C). Time-density curves were obtained from digital angiograms of the myocardial region of interest. We measured peak contrast density (Cm) and time to peak contrast (Tm). An index of rMFR was calculated as the quotient of Cm/Tm before and after P. In HCM, rMFR in IVS and apex was significantly lower than that of C (Mid-IVS: 1.9 +/- 0.5 vs 3.9 +/- 0.5, p less than 0.001; Low-IVS: 2.0 +/- 0.5 vs 4.4 +/- 0.9, p less than 0.001; Apex: 2.0 +/- 0.7 vs 4.5 +/- 1.6, p less than 0.01). There was correlation between the impairment of rMFR and the extent of hypertrophy in HCM. In conclusion, we could state that, in HCM, the region of impaired myocardial coronary blood flow reserve is localized. In HCM, DSA is useful in evaluating myocardial coronary blood flow reserve.
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PMID:[Regional myocardial coronary blood flow reserve in hypertrophic cardiomyopathy assessed by digital subtraction coronary angiography]. 226 32


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