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

Exercise Tl scintigraphy (EX-Tl) provides a noninvasive means of identifying myocardial perfusion abnormalities in patients (pts) with hypertrophic cardiomyopathy (HCM). We have noted that some pts with HCM have a pattern of transient dilation of the left ventricle (LV) on the immediate post exercise images as compared with 3 hour redistribution images. We presumed that left ventricular dilation was caused by subendocardial hypoperfusion. So we studied transient dilation of the LV in 50 pts with HCM and 20 controls (C). Initial and delayed conventional short tomographic images were obtained after reconstruction of 30 projections acquired over 180 degrees. Thirty six radii every 10 degrees were generated from the center of the middle myocardial images of the short axis. An area surrounded by the thirty six points of maximal count on each radius was calculated in initial and delayed images. Transient Dilation Index (TDI) as an index of dilation was determined by dividing an area in initial image by an area in delayed image. TDI in pts with HCM was larger than that in C. Pts with HCM were classified into the two groups, Group A: TDI greater than 1.11 (mean + 2 SD in C), 24 pts, Group B: TDI greater than 1.11, 26 pts. Frequency of pts with history of chest pain in Group A was higher than that in Group B, and frequency of pts with positive exercise ECG in Group A was higher than that in Group B. End diastolic volume in Group B did not change 10 minutes after exercise by radionuclide ventriculography. In conclusion, transient dilation of the LV in pts with HCM by EX-Tl is in appearance, and may reflect subendocardial ischemia.
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PMID:[Assessment of transient dilation of the left ventricular cavity in patients with hypertrophic cardiomyopathy by exercise thallium-201 scintigraphy]. 229 Jan 96

The usefulness of cardiac ultrafast computed tomography (CT) is discussed in this article. Thirty-three patients with ischemic heart disease and 15 patients with hypertrophic cardiomyopathy were assessed for myocardial characteristics, while 30 patients with various heart diseases were assessed for cardiac function. Volume mode (100 msec scan) and cine mode (50 msec scan) studies were applied. As the findings of abnormal myocardial characteristics, early defect (ED) and late enhancement (LE) of the left ventricular (LV) wall were observed after injection of contrast medium. In ischemic heart disease, all 27 patients with myocardial infarction (MI) and all 16 MI sites showed LE, while 25 ED sites were well correlated with MI or significant coronary stenosis. LE was quite sensitive for MI and ED was highly predictive for ischemia. Seven of 15 HCM patients (47%) also showed LE, indicating that LE occurs in tissues with a different capillary architecture from that observed in normal myocardium. For evaluation of cardiac function, ventricular volumetry was performed by summation of a sliced area of the ventricles. End-diastolic volume and LV ejection fraction calculated by this means correlated excellently with the values obtained using left ventriculography (R = 0.97 and 0.96). The stroke volumes for both ventricles were nearly equal when calculated using ultrafast CT. Consequently, the study of cardiac volumetry using ultrafast CT was thought to be reliable and utilizable in clinical practice.
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PMID:Significance of ultrafast computed tomography in cardiac imaging: usefulness in assessment of myocardial characteristics and cardiac function. 236 18

The hemodynamic effects of cardiac pacing at different rates and in different modes were studied in 21 patients who were candidates for permanent pacemaker implantation. Nine of these had primary conduction disturbances (PCD), ten had ischemic heart disease (IHD), seven with additional cardiac failure (CHF), and two had hypertrophic cardiomyopathy (HCM). In patients with PCD, atrial (AOO) and AV sequential (DVI) pacing did not change systolic blood pressure and pulse pressure but ventricular (VVI) pacing caused a progressive fall in these measurements, especially as heart rate increased. Ventricular volume and stroke volume (counts) derived from radionuclide ventriculography (RVG) decreased progressively with higher pacing rates, especially during VVI pacing. Cardiac output was maintained during VVI pacing by the increase in heart rate; during AOO and DVI pacing, cardiac output increased. Similar but more marked differences were observed in patients with IHD and CHF and the changes were even greater in the patients with HCM. Left ventricular (LV) ejection fraction changed little with increasing heart rate in PCD but decreased progressively with the onset of ischemia in IHD and CHF. There was no difference in ejection fraction in the different pacing modes. Graphs related to LV contractility (end-systolic pressure-volume relations) showed that AOO pacing produced the highest and VVI pacing produced the lowest curves of myocardial contractility in all patient groups, except that at higher rates the AOO curve shifted down again in patients with IHD and CHF, presumably with the onset of myocardial ischemia. This study showed that physiological pacing produced the best hemodynamic results in all patient groups. Higher pacing rates should be avoided in patients with ischemic heart disease while VVI pacing should not be used in patients with HCM. Blood pressure and RVG studies during temporary pacing are useful in selecting the optimal pacing system in an individual patient when the clinical choice is not clear.
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PMID:Left ventricular function during physiological cardiac pacing: relation to rate, pacing mode, and underlying myocardial disease. 243 37

Impaired left ventricular relaxation and filling is an important pathophysiologic mechanism in hypertrophic cardiomyopathy. To determine whether isoproterenol, known to improve relaxation in isolated cardiac muscle, could favorably modify this effect, we assessed simultaneous left ventricular volume and regional systolic asynchrony (by radionuclide angiography), left ventricular pressure (by micromanometer catheters), and lactate metabolism in 12 patients with hypertrophic cardiomyopathy. Pressure-volume relations were studied during atrial pacing stress to induce myocardial ischemia and during isoproterenol infusion to similar heart rates. Angina occurred in 10 patients with pacing and in 11 patients during isoproterenol infusion; lactate consumption was reduced in nine patients during isoproterenol compared with pacing, including five patients who produced lactate with isoproterenol. During isoproterenol compared with pacing, peak left ventricular pressure was higher (205 +/- 33 vs. 142 +/- 21 mm Hg, p less than 0.001), ejection fraction was higher (77 +/- 10% vs. 71 +/- 12%, p less than 0.02), and regional systolic nonuniformity was diminished. Despite ischemia, these changes in load and nonuniformity during isoproterenol were associated with enhanced diastolic function compared with pacing tachycardia: isoproterenol reduced T 1/2, the half-time of pressure decline after peak negative dP/dt (from 46 +/- 10 to 33 +/- 6 msec, p less than 0.001), shifted the diastolic pressure-volume curve downward and rightward in 10 of 12 patients, and increased end-diastolic volume (from 77 +/- 18% to 100 +/- 11% of control values, p less than 0.001) with no change in end-diastolic pressure (19 +/- 7 to 19 +/- 5 mm Hg, p = NS). Thus, despite ischemia, isoproterenol improved left ventricular relaxation and filling compared with tachycardia in the absence of beta-adrenergic stimulation. Although isoproterenol is detrimental in hypertrophic cardiomyopathy by provoking ischemia, these data suggest that the adverse effects of ischemia on ventricular relaxation and distensibility may be alleviated by beta-adrenergic stimulation, possibly as a result of enhanced inactivation and restored load sensitivity.
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PMID:Beta-adrenergic stimulation with isoproterenol enhances left ventricular diastolic performance in hypertrophic cardiomyopathy despite potentiation of myocardial ischemia. Comparison to rapid atrial pacing. 253 98

From 1982 to 1986, 1230 sudden death cases were autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were sudden cardiac deaths (SCD) including coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours of the appearance of the fatal symptoms, and most of them (72%) were considered instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%), or at work (8%). Thirty-four percent of them were thought by themselves or by their families to be healthy before the death. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were the major past history recorded. Microscopic observation of the hearts of 200 cases autopsied in 1986 showed various cardiac lesions: hypertrophy, atrophy, degenerations of myocytes, cellular and fatty infiltrations of the interstitium. According to their cardiac lesions and degrees of severity of coronary sclerosis, patients who died suddenly were divided into 8 groups as follows: 1. myocardial infarction (41) 2. myocarditis (6) 3. hypertrophic cardiomyopathy (19) 4. chronic ischemia with severe coronary sclerosis (65) 5. chronic ischemia with moderate coronary sclerosis (27) 6. small vessel disease (18) 7. amyloidosis (1) 8. unknown (23). These results suggest that coronary heart disease and hypertension play an important role in SCD.
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PMID:An epidemiologic and histopathological study of sudden cardiac death in Osaka Medical Examiner's Office. 263 29

Previous observations and clinical manifestations suggest the presence of ischemia in the disproportionately thickened septum of patients with hypertrophic cardiomyopathy. Metabolic consequences of ischemia can be demonstrated with positron emission tomography. Therefore, 10 patients with hypertrophic cardiomyopathy and an echocardiographic septum to posterior wall thickness ratio of 1.8 +/- 0.4 cm (range 1.3 to 2.5) were studied with the use of nitrogen (N)-13 ammonia, carbon (C)-11 palmitate and fluoro (F)-18 2-deoxyglucose as tracers of myocardial blood flow, fatty acid metabolism and exogenous glucose utilization. The results of positron emission tomography in 9 patients with hypertrophic cardiomyopathy were compared with those in 10 normal volunteers. In the hypertrophic cardiomyopathy group, observed myocardial activity of N-13 ammonia and C-11 palmitate in the septum was similar to that in the lateral wall. Septum to lateral wall tissue activity ratios averaged 1.04 +/- 0.15 for N-13 ammonia and 1.04 +/- 0.18 for C-11 palmitate, and were similar to those in the normal volunteers (0.98 +/- 0.07 and 0.98 +/- 0.03, respectively; p = NS). Myocardial clearance half-time and residual fraction of C-11 palmitate did not differ significantly between the septum and lateral wall. However, F-18 2-deoxyglucose uptake was significantly lower in the septum than in the lateral wall (15,768 +/- 4,314 versus 19,818 +/- 5,234 counts/pixel; p less than 0.003). The mean septum to lateral wall activity ratio of 0.83 +/- 0.21 was less than that observed in normal volunteers (0.92 +/- 0.07; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional myocardial blood flow and metabolism at rest in mildly symptomatic patients with hypertrophic cardiomyopathy. 252 4

Standard methods of echocardiographic analysis permit accurate categorization of cardiomyopathies into dilated, hypertrophic, and restrictive types. However, ascertainment of the cause of a particular cardiomyopathy (e.g., ischemia versus inflammation as the cause of a dilated myopathy) with ultrasound would be greatly facilitated by analysis of myocardial composition with ultrasound tissue characterization techniques. Qualitative observations have identified unusual echocardiographic image texture in hypertrophic cardiomyopathy and in amyloidosis. Quantitative observations have verified these findings and have identified increased ultrasound backscatter in regions of myocardial fibrosis, calcification, and anthracycline-induced cardiomyopathy. Although several technical problems remain unsolved and further research is needed in the mechanisms of normal and abnormal ultrasound/tissue interactions, tissue characterization with ultrasound has the potential to contribute independent information on myocardial composition in patients with cardiomyopathy.
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PMID:Clinical potential of ultrasound tissue characterization in cardiomyopathies. 307 43

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic entity that involves principally the left ventricle and is caused by asymmetric or concentric hypertrophy of unknown cause. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the apex, at the midventricular level, or, rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by upper septal hypertrophy narrowing the outflow tract and setting the stage for Venturi forces to cause systolic anterior motion of the anterior or posterior mitral leaflets. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyotomy-myectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. This form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy available today. The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness (decreased compliance) that characterize diastole in hypertrophic cardiomyopathy. Relaxation is impaired by the contraction load (the obstruction), by a decrease in the principal relaxation loads, by a pathologic degree of nonuniformity of contraction and relaxation, and in all likelihood, by impaired inactivation of the biochemical processes responsible for contraction (? due to primary or ischemia-induced calcium overload). Calcium channel-blocking agents may dramatically improve left ventricular relaxation by speeding up the inactivation process, by decreasing the degree of nonuniformity, or by altering the contraction and relaxation loads in a favorable manner. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their occurrence also appears to depend on the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole as well as the disturbances of rhythm appear to be related to the site and/or extent of the hypertrophic process.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review. 316 67

While the total ischemic burden on the left ventricle represents the combined effects of both symptomatic and asymptomatic myocardial ischemia, the total vascular burden has many components including an increased systemic peripheral vascular resistance, an increased pulmonary vascular resistance, and an increased coronary vascular resistance. These factors may all influence ventricular function. Hypertension contributes significantly to the vascular burden, especially when combined with left ventricular hypertrophy, which predisposes to ischemia by multiple mechanisms. In patients with hypertension and cardiomegaly, sublingual nifedipine has been shown to increase left ventricular (LV) ejection fraction and the average diastolic filling rate. In the presence of acute myocardial infarction, nifedipine moves the LV function curve onto a better Frank-Starling relationship as pulmonary wedge pressure falls or stays the same and cardiac output rises. However, because of the delicate balance between myocardial perfusion and the benefits of afterload reduction, including improved remodelling, nifedipine should be given only to selected patients. In congestive heart failure, low-dose nifedipine reduces the afterload and has been shown to have beneficial effects in the majority of patients. Two specific adverse outcomes in only two patients have been reported, one with initial hypotension and one given high-dose nifedipine. Combination nifedipine-beta blocker therapy has been shown to be favorable in the treatment of all varieties of angina, hypertension, and hypertrophic cardiomyopathy. Therefore, when administered appropriately, nifedipine reduces the total vascular burden on the heart in a variety of cardiovascular diseases, with consequent improvement in LV function and a diminished threat of potential myocardial ischemia.
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PMID:The total vascular burden, peripheral and coronary: vasodilator effects of nifedipine. 327 10

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease of unknown cause that is characterized by a hypertrophied, nondilated, hypercontractile left ventricle. Its etiology and pathogenesis remain undefined but the three principal factors implicated are a genetic predisposition, a hypersensitivity to catecholamines, and an abnormal calcium metabolism. The hypertrophy typically involves the intraventricular septum to varying degrees, but may also involve the apex or free wall and even be concentric. The disease occurs in either an obstructive or a nonobstructive form depending on whether an intraventricular pressure gradient can be demonstrated at rest or on provocation. The gradient and obstruction to outflow is usually seen in patients with asymmetric septal hypertrophy (ASH) and anterior motion of the mitral valve during systole (SAM). Abnormal left ventricular diastolic function characterized by inadequate filling and impaired relaxation has been shown to be very important in both the obstructive and nonobstructive forms of the disease. In addition, inadequate coronary vasodilator reserve as a result of small vessel disease, microvascular spasm, and/or low capillary density per unit myocardial mass has been implicated as an important cause of ischemia in patients without coronary artery disease. HCM is a disease of young adulthood with relatively slow progression; young patients are often asymptomatic, whereas older patients are more limited by dyspnea, angina, dizziness, or syncope. Supraventricular tachyarrhythmias occur in 30% of patients, and high-grade ventricular arrhythmias occur in over 75%. The annual mortality is 3-5%. The common mode of demise is sudden cardiac death. Therefore, the primary objectives of treatment are the amelioration of symptoms, the control of arrhythmias, and the prevention of sudden death. Beta-adrenoreceptor blocking agents decrease myocardial contractility and oxygen demands and increase ventricular volume; therefore, they are most useful in patients with the obstructive form of HCM. Calcium channel antagonists enhance left ventricular relaxation, relieve microvascular spasm, and improve coronary filling and therefore are the agents of choice in patients with diastolic dysfunction. The ability of the calcium channel antagonists to decrease contractility makes them valuable in patients with obstructive HCM. Arterial vasodilators, diuretics, nitrates, and inotropic agents should be avoided because they can increase the intraventricular gradient. Myomyectomy is reserved for those patients with the obstructive form of HCM whose symptoms are refractory to medical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy: current views on etiology, pathophysiology, and management. 331 Jun 37


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