Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of aortic valve stenosis without coronary artery disease was confirmed to have diffuse subendocardial ischemia by exercise Thallium-201 myocardial single photon emission computed tomography. A 72-year-old woman, who had been diagnosed as aortic valve stenosis, was admitted because of chest pain during exercise. In cardiac catheterization findings, the patient angiographically had normal coronary arteries and no asynergy of left ventricular wall motion. The peak flow velocity in continuous wave Doppler echocardiography was about 5.0 m/sec at aortic valve level, providing a pressure drop of 100 mmHg across a stenotic valve with calculating on a modified Bernoulli equation (PG = 4V2). Thallium-201 myocardial SPECT images during exercise showed a transient "dilation and a widespread wall thinning" of left ventricle with apical perfusion defect. Simultaneous electrocardiogram showed further ST depression and the patient had chest pain. In 6 months after aortic valve replacement the patient no longer demonstrated both apical perfusion defect and "wall thinning" in postoperative thallium-201 myocardial SPECT images and also had neither ST depression nor chest pain. Thus; a transient "dilation and wall thinning" of left ventricle in this patient is suspected to be a sign of diffuse subendocardial ischemia.
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PMID:[Diffuse subendocardial ischemia in a patient with aortic valve stenosis without coronary artery disease by exercise 201Tl SPECT]. 157 26

Patients with heart disease may have myocardial ischemia or left ventricular (LV) dysfunction without symptoms. The exercise responses of 14 asymptomatic patients with valvular aortic stenosis (AS) were studied using treadmill testing, thallium-201 scintigraphy and radionuclide angiography. Compared with age- and gender-matched control subjects, patients with AS demonstrated reduced exercise tolerance (10.7 +/- 2.5 vs 13.3 +/- 4.2 min; p = 0.06) and maximal oxygen consumption (26.7 +/- 6.3 vs 36.3 +/- 9.5 ml O2/min/kg; p = 0.004) associated with decreased peak systolic blood pressure response to exercise (177 +/- 18 vs 214 +/- 42 mm Hg; p less than 0.004). Ten of 14 patients developed ST-segment depression during exercise, only 3 of whom had reversible thallium defects. Patients with AS tended to have greater LV ejection fractions at rest (65 +/- 11 vs 58 +/- 7; p = 0.08) and significantly decreased early peak filling rates (4.8 +/- 1.3 vs 6.1 +/- 0.6 stroke volume/s; p = 0.003) compared with those of control subjects. During maximal supine exercise, patients with AS had less of an increase in ejection fraction (2 +/- 9 vs 15 +/- 7%; p less than 0.001) associated with a decrease in end-diastolic (-7 +/- 15 vs +5 +/- 16%; p = 0.06) and stroke (-6 +/- 17 vs +30 +/- 13%; p less than 0.001) volumes from baseline measurements.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic and left ventricular responses to exercise stress in asymptomatic patients with valvular aortic stenosis. 174 29

The aim of this study was to determine the effect of low-pressure and high-pressure reperfusion, with and without ventricular fibrillation, on the recovery of hypertrophic and normal hearts after hypothermic cardioplegia. Fourteen hearts rendered hypertrophic by valvular aortic stenosis and 18 normal canine hearts were subjected to 1 hour of cardioplegic arrest at 28 degrees C during cardiopulmonary bypass. Each heart was then reperfused at a coronary pressure of either 40 mm Hg (low) or 80 mm Hg (high), initially in the empty beating state and then during ventricular fibrillation. Low-pressure reperfusion produced left ventricular subendocardial ischemia in hypertrophic and in normal hearts, shown by marked depression of subendocardial blood flow, myocardial pH, and myocardial oxygen consumption. In hypertrophic hearts the ischemia was more severe and resulted in a persistent depression of left ventricular function and myocardial oxygen consumption even when coronary pressure was returned to normal levels. High-pressure reperfusion was associated with rapid and complete recovery of myocardial metabolism and function in hypertrophic and in normal hearts. During low-pressure reperfusion, ventricular fibrillation exacerbated ischemia in hypertrophic and in normal hearts. During high-pressure reperfusion, a short period of ventricular fibrillation produced no adverse effects either in hypertrophic or in normal hearts. We conclude that low-pressure reperfusion produces subendocardial ischemia in normal and in hypertrophic hearts even in the empty beating state; in hypertrophic hearts it also impairs recovery of myocardial metabolism and function. The adverse effects of low-pressure reperfusion are exacerbated by ventricular fibrillation.
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PMID:Adverse effects of low-pressure reperfusion after hypothermic cardioplegia in normal and hypertrophic hearts. 183 91

We compared the activity and physiologic effects of cardiac angiotensin converting enzyme (ACE) using isovolumic hearts from male Wistar rats with left ventricular hypertrophy due to chronic experimental aortic stenosis and from control rats. In response to the infusion of 3.5 X 10(-8) M angiotensin I in the isolated buffer perfused beating hearts, the intracardiac fractional conversion to angiotensin II was higher in the hypertrophied hearts compared with the controls (17.3 +/- 4.1% vs 6.8 +/- 1.3%, P less than 0.01). ACE activity was also significantly increased in the free wall, septum, and apex of the hypertrophied left ventricle, whereas ACE activity from the nonhypertrophied right ventricle of the aortic stenosis rats was not different from that of the control rats. Northern blot analyses of poly(A)+ purified RNA demonstrated the expression of ACE mRNA, which was increased fourfold in left ventricular tissue obtained from the hearts with left ventricular hypertrophy compared with the controls. In both groups, the intracardiac conversion of angiotensin I to angiotensin II caused a comparable dose-dependent increase in coronary resistance. In the control hearts, angiotensin II activation had no significant effect on systolic or diastolic function; however, it was associated with a dose-dependent depression of left ventricular diastolic relaxation in the hypertrophied hearts. These novel observations suggest that cardiac ACE is induced in hearts with left ventricular hypertrophy, and that the resultant intracardiac activation of angiotensin II may have differential effects on myocardial relaxation in hypertrophied hearts relative to controls.
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PMID:Increased rat cardiac angiotensin converting enzyme activity and mRNA expression in pressure overload left ventricular hypertrophy. Effects on coronary resistance, contractility, and relaxation. 217 12

Regional stress-velocity relations were determined in a first group of patients (n = 15) with normal (five controls, five patients with aortic stenosis, and five patients with aortic insufficiency) and a second group of patients (n = 10) with depressed contractility (five patients with aortic stenosis and five with aortic insufficiency). LV circumferential wall stress was calculated from high-fidelity pressure and frame-by-frame angiocardiographic data using the Wong thick-wall model. Regional wall stress and shortening velocity were calculated from the endo- to the epicardium, and from the equator to the apex at 35 points. Regional LV wall stress was in all patients lower at the epi- than the endocardium, and lower at the apex than the equator. Regional stress-velocity relations were downward shifted from the endo- to the epicardium and from the equator to the apex (family of curves) in both groups. At corresponding LV regions stress-velocity relations showed significantly smaller slopes and intercepts (downward depression) in group 2 than in group 1. Thus, wall stress distribution is inhomogeneous in the normal, as well as in the pressure and volume overloaded left ventricle. Regional differences in stress-velocity relations within groups (family of curves) are probably related to changes in preload rather than to changes in regional contractility. Downward depression of the regional stress-velocity relations in group 2 is caused by depressed myocardial contractility.
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PMID:Left ventricular wall stress distribution in chronic pressure and volume overload: effect of normal and depressed contractility on regional stress-velocity relations. 224 67

A 38-year-old man was referred to our hospital because of a heart murmur and mild fever. Physical examination disclosed a systolic murmur of grade 3/6 at the apex and a diastolic murmur of grade 4/6 at the 2nd intercostal space of the left sternal border. The chest radiograph revealed mild cardiomegaly. The ECG showed left ventricular hypertrophy and ST segment depression in leads I, aVL and V4 to V6. Aortogram demonstrated supravalvular aortic stenosis (SAS) and aortic regurgitation. At the operation, we found the right coronary ostium was severely narrowed by the thickened right coronary cusp and the fibrous ring causing SAS. Aortic valve replacement and extended aortoplasty were performed. He had been doing well but suddenly died 11 months after the operation.
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PMID:[An operated case of supravalvular aortic stenosis and aortic regurgitation and narrowed right coronary ostium]. 235 2

In hypertensive heart disease without coronary artery disease it has been proposed that the presence of ischemia of myocardial tissue is due to an inadequate increment of myocardial mass or to an increase in coronary artery resistance. In this study, 18 patients with aortic stenosis, without coronary artery disease were included. It was demonstrated that the existence of myocardial ischemic, induced by atrial pacing and manifested by ST segment depression, had direct association to increased myocardial mass, and it had no relation with left ventricular telediastolic pressure nor with transvalvular gradient. The results support the hypothesis that an inappropriate increment of the myocardial mass is the main cause of myocardial ischemia in these type of cardiopathies.
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PMID:[Myocardial ischemia in aortic stenosis]. 253 25

The morphological and functional aspects of the left ventricle (LV) were assessed by echocardiography and cardiac catheterization performed simultaneously in 41 patients. Eleven were normal (N), 14 had aortic stenosis (AS) and 16 had aortic regurgitation (AR). Of the 14 patients with AS, eight were in New York Heart Association (NYHA) functional class I and II (ASA group) and six were in NYHA functional class III and IV (ASB group). Of the 16 patients with AR, seven were in NYHA functional class I and II (ARA group) and nine in functional class III and IV (ARB group). In the ASA group normal values of the LV function were obtained because of the development of an adequate hypertrophy that in normalizing the systolic stroke was able to keep a suitable function. In the ASB group there was a reduction of the LV function due to an increase of the systolic stroke and to the reduction of the contractile muscle state. Thus, in the whole AS group we found an inversed relation between the ejection fraction and the systolic stroke. In the ARA group we found a normal cardiac function as consequence of an adequate development of the LV dilation and hypertrophy. Despite the find of reduction of the contractile state, the systolic stroke normalizing was capable to keep the cardiac function at normal values. The ARB group presented an important depression of the cardiac function due the increase of the systolic stroke and to the decrease of the contractile state of the cardiac muscle.
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PMID:[Analysis of the mechanical properties of the left ventricle in patients with aortic valve disease]. 263 9

A sixty-six-year-old man with severe aortic stenosis, in whom simultaneous and continuous monitoring of the electrocardiogram and arterial blood pressure was performed immediately before, during, and following recovery from exercise-induced syncope, is reported. During exercise the patient developed anginal pain associated with a gradual fall of arterial blood pressure followed by syncope. At the onset of the syncope, arterial blood pressure was extremely low, and the electrocardiogram showed sinus tachycardia. It was assumed from these findings that profound hypotension, induced by peripheral vasodilatation and ischemic myocardial depression leading to inappropriately low cardiac output, was the underlying factor mainly responsible for the occurrence of exercise-induced syncope in the present case.
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PMID:Simultaneous monitoring of electrocardiogram and arterial blood pressure during exercise-induced syncope in a patient with severe aortic stenosis--a case report. 291 63

In aortic valve stenosis, concentric hypertrophy develops which is characterized by a reduced end-diastolic radius-to-wall thickness ratio (r/h) with an essentially normal cavity shape. As long as the product of (r/h) and LV systolic pressure remains constant, hypertrophy is appropriate. An increase in the product, which represents an increase in wall stress signals inadequate LV hypertrophy. Although at first glance, massive LV hypertrophy appears favourable for the maintenance of a normal LV ejection fraction in aortic stenosis, data from 23 studies of the literature have shown an inverse relationship between ejection fraction and LV angiographic mass m-2 (r = -0.59). Both a degree of hypertrophy inadequate to keep systolic wall stress within normal limits and a reduction of LV contractility may explain the depression of ejection fraction when LV angiographic mass is sizeably increased. Conversely, a normal ejection fraction in aortic stenosis may not be indicative of normal systolic myocardial function under all circumstances. In the presence of mildly reduced contractility, a normal ejection fraction may be maintained by the use of preload reserve. Assessment of myocardial structure from LV endomyocardial biopsies revealed no differences in muscle fibre diameter, interstitial fibrosis and volume fraction of myofibrils between patients with aortic stenosis having a normal and those with a depressed ejection fraction. Preoperative ejection fraction is a poor predictor of postoperative survival, whereas markedly increased preoperative angiographic mass and end-systolic volume have been reported to predict an unsatisfactory postoperative outcome characterized by either death or poor LV function.
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PMID:Left ventricular systolic function in aortic stenosis. 296 11


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