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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

To determine the serial changes in T1 and T2 relaxation times of myocardial infarction, and their relationship to observed changes in water content, regional myocardial blood flow, and histopathology, rabbits were studied at 14 time intervals ranging from 30 min to 6 months after coronary artery ligation. All values were compared to a control group. Hearts were subdivided into infarct and normal segments for measurement of blood flow, water content, and relaxation times (20-MHz spectrometer); other hearts were excised intact for histopathologic studies. T1 relaxation time of infarcted myocardium did not change significantly compared to control over the 6-month study period. T2 relaxation time increased (P less than 0.0001) at 3 days and returned to baseline by 2 months. Consonant with the increase in T2 of infarct, nuclear magnetic resonance (NMR) images at 3 days demonstrated an increase in signal intensity of infarct compared to surrounding normal myocardium. At 6 months, marked myocardial thinning was observed without changes in signal intensity. Changes in T2 of infarcted myocardium were not related to changes in water content or severity of ischemia, but correlated best with infarct healing and scar formation as detected on histopathology. In conclusion, the findings of this study indicate that T2 relaxation time of the infarcted myocardium increases markedly at 3 days and remains elevated for 2 months. These changes correlate best with the onset and progression of infarct healing. These data demonstrate the potential of T2-weighted NMR imaging for assessing healing patterns following ischemic myocardial injury.
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PMID:Serial changes in nuclear magnetic resonance relaxation times after myocardial infarction in the rabbit: relationship to water content, severity of ischemia, and histopathology over a six-month period. 323 Oct 66

Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.
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PMID:[Experimental mitral regurgitation in ischemia-induced papillary muscle dysfunction]. 325 3

The authors describe their personal experience using Magnetic Resonance Imaging (MRI) in the evaluation of cardio-vascular diseases. MRI made it possible to obtain multiplanar anatomical images of the cardio-vascular system without X-rays and conventional contrast medium. MRI supplied with indirect flow evaluation, too. MRI was particularly useful in the assessment of congenital heart diseases, since it shows the heart chambers and the great vessels at the same time and in the different phases of cardiac revolution. MRI was also useful in the evaluation of many acquired heart diseases, such as myocardium diseases, valve diseases, myocardial ischemias, pericardium diseases. Moreover, MRI correctly showed aortic aneurysms. In all the 55 patients examined, it was possible to obtain a good definition of the cardiac structures, especially when "cardiac gating" was employed. In the 3 ventricular and in the 5 atrial defects, the dimensions of the defect and the dilatation of the involved cardiac chambers were precisely assessed. In the 6 aortic coarctations, MRI evaluated the level and the grade of the stenosis, with consequent definition of the anatomic type. Moreover, collateral circulation and dilatation before and/or after the stenosis were evident. In all the 7 complex cardiopathies examined (3 Fallot tetralogies, 1 Fallot pentalogy, 1 aortic cervical arch, and 2 Ebstein diseases) MRI demonstrated each single anomaly of the malformations, at both cardiac and vascular levels. In 2 patients with atrial fibrillation, MRI visualized endoatrial thrombi. In the 7 patients with previous myocardial infarction, the site of ischemia was depicted as a thinning of the wall, while the remaining myocardium appeared hypertrophic. MRI correctly demonstrated all thoracic aorta aneurysms, even in a case where both CT and angiography were negative, due to the aneurysm being thrombosed. Mural thrombi were evident with both MRI and CT, but not always visible with angiography. In the 5 dissected aneurysms, MRI--like CT--assessed the origin of the dissection, and the dimensions of the true and false lumen; moreover, it indirectly evaluated the slow and turbulent blood flow within the true lumen, and the presence of thrombi in the false lumen.
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PMID:[Use of magnetic resonance in the diagnosis of congenital and acquired cardiopathies. Preliminary note]. 337 87

Left ventricular dimensions, wall thickness, wall stress, and indexes of afterload, preload, contractility, and early diastolic function, as well as regional wall motion, were determined by echocardiographic methods in patients with transposition of the great vessels after arterial switch operation and in age-matched normal controls. In patients evaluated early after surgery, body surface area-adjusted left ventricular dimensions were smaller, and wall thickness was increased compared with controls. Ventricular performance (fractional shortening) was normal in most patients but was abnormally low in 10%. Nevertheless, contractility was normal or augmented in all subjects, with a mean value higher than the control group. The reduction in systolic function was related to altered loading conditions with a combination of reduced afterload and preload combined with augmented contractility. These altered myocardial mechanics appeared to be secondary to routine therapy with digitalis and diuretics. Diastolic function was also normal with differences in the rate of peak filling and rate of wall thinning entirely attributable to differences in ventricular size and function, and normalized indexes of diastolic function were not different between patients and controls. Patients evaluated late after repair were found to have normal regional wall motion with no evidence to suggest regional dysfunction as might be seen with regional ischemia. Ventricular size, wall thickness, systolic function, afterload, preload, contractility, and early diastolic function were indistinguishable from control values. Indexes of diastolic function demonstrated the same relation to age, body surface area, and ventricular size and function in both patients and controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial performance after arterial switch operation for transposition of the great arteries with intact ventricular septum. 338 97

Positron emission tomography (PET) with rubidium-82 (82Rb) has been developed to measure regional myocardial perfusion and to detect transient ischemia both in the experimental laboratory and in humans. There are known and separate contaminating effects of the 82Rb signal by disturbances in wall motion, wall thinning, and the partial volume effect that occur during transient ischemia. In nine anesthetized greyhounds, PET with 82Rb (T1/2 = 78 sec) was used to determine the regional myocardial uptake of this cation during a control period that consisted of a mild stenosis of the left anterior descending coronary artery in the absence of ischemia (to limit reactive hyperemia), during 10 min of total occlusion and, finally, at 30 and 60 min of recovery with release of the occlusion but not of the stenosis. Separately, rubidium-81 (81Rb); T1/2 = 4.58 hr) was given as a peripheral intravenous injection 2 hr before the study to allow this long-lived tracer to distribute in the potassium space of the myocardium. Observations during control and ischemia revealed marked decreases in 82Rb uptake (0.84 +/- 0.12 to 0.28 +/- 0.12, p = 0.001) in affected regions and were paralleled by similar decreases in microsphere blood flow (0.88 +/- 0.08 to 0.12 +/- 0.10 ml/min/g, p = 0.003), which gradually recovered by 60 min postischemia. Lesser decreases in 81Rb activity (0.84 +/- 0.11 to 0.76 +/- 0.17, p = 0.83) were observed in the same regions during ischemia, but these were immediately reversible. Separate in vitro postmortem experiments in eight rabbits confirmed a linear relationship between plasma and myocardial activities of stable potassium and 81Rb although there was a greater concentration of 81Rb in the myocardium that in the plasma relative to potassium (y = -3.29 +/- 0.79 x, s.e.e. 1.91, r = 0.95). These studies demonstrate that if 81Rb is given intravenously to distribute into the potassium pool, tomograms of the heart may be recorded to measure the potassium-rich mass of myocardium providing information about the acute effects of wall thinning during ischemia. Rubidium-81 used in this way may be helpful in assessing the effects of wall thinning and/or scar when other tracers are being used to assess perfusion or metabolism.
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PMID:Use of short- and long-lived rubidium tracers for the study of transient ischemia. 349 48

Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last drug-induced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.
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PMID:Effect of repeated episodes of drug-induced ventricular dyskinesia on subsequent regional function in the dog: comparison with myocardial stunning produced by repeated coronary occlusions. 358 22

The relative time courses of early changes in myocardial metabolism and function during anoxia, global ischemia, and regional ischemia were compared in isolated rat hearts. Transmural anoxic wave front was determined with NADH fluorescence photography, and oxygen saturation of myoglobin and dynamic systolic wall thickening were measured with spectrophotometry of light transmitted through the left ventricular free wall. In all three treatments, anoxic wave front first appeared in the subendocardium and reached the epicardial half of the myocardium in 10 s, when oxygen saturation of myoglobin decreased by 50% and tissue ATP and creatine phosphate remained at aerobic levels. During this period, systolic wall thickening decreased gradually in anoxia and global ischemia, whereas a marked decrease in systolic wall thickening and appearance of dyskinesia (wall thinning) occurred in regional ischemia. Thus the early extension of anoxic wave front and metabolic changes are similar with all three treatments, and dyskinesia, observed only in case of regional ischemia, occurs when the inner half is ischemic or anoxic.
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PMID:Transmural anoxic wave front and regional dysfunction during early ischemia. 361 98

It is hypothesized that myocardium subjected to a 5 minute period of coronary occlusion and a 30 minute period of reperfusion has latent abnormalities that become overt when the reperfused myocardium is "challenged" by a subsequent coronary occlusion. This hypothesis is clinically relevant because reperfused myocardium is frequently subjected to recurrent ischemia, as in patients with unstable angina, vasospastic angina or recurrent thrombosis after initial coronary occlusion and thrombolysis. In 19 open chest dogs, the response of regional myocardial function to brief coronary occlusions was studied. Systolic wall thickening and diastolic thinning were measured using a specially developed miniature 5 MHz echocardiographic transducer fixed to the epicardium by suction. All 19 dogs underwent an initial "challenge" coronary occlusion (30 seconds). Thereafter, the control group (n = 8) underwent no intervention for 30 minutes, while the intervention group (n = 11) underwent 5 minutes of coronary occlusion followed by 30 minutes of reperfusion. All dogs were then subjected to a second "challenge" coronary occlusion (30 seconds). In the control group, responses to the second challenge occlusion were the same as to the first occlusion. In the intervention group, regional and global systolic function and myocardial perfusion after the 5 minute coronary occlusion intervention returned to baseline levels, but the response to the second challenge coronary occlusion was significantly different in the intervention group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered response of reperfused myocardium to repeated coronary occlusion in dogs. 365 54

To investigate the mechanism of the depression of left ventricular (LV) peak negative dP/dt during acute regional ischemia, studies were performed in seven open-chest anesthetized dogs. Regional LV wall thickness was measured with ultrasonic crystals in both an ischemic and a normally perfused segment. Ischemia was produced by complete occlusion of the left anterior descending coronary artery for 30 seconds. Within 10 seconds of ischemia, premature thinning of the ischemic wall developed, which preceded thinning of the normal LV wall by 100 +/- 20 msec. Premature thinning of the ischemic segment was associated with 29% reduction of peak negative dP/dt, a 29% prolongation of LV isovolumic relaxation time, and a 15% reduction of the LV systolic ejection period. We offer the following explanation for the depression of LV peak negative dP/dt. 1. Peak negative dP/dt is depressed as a result of a prolongation of the isovolumic relaxation time. 2. The isovolumic relaxation time is prolonged as a result of shortening of the systolic ejection period. 3. Shortening of the systolic ejection period is mediated by an early fall of LV systolic pressure caused by inability of the LV to sustain systolic pressure. 4. Inability of the LV to sustain systolic pressure is caused by premature thinning of the ischemic region during late systole.
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PMID:Proposed mechanism for depression of maximal rate of left ventricular pressure fall (peak negative dP/dt) during regional myocardial ischemia. 373 Dec 66


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