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 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The studies reported here were selected because of renewed interest in these areas, particularly as they relate to the evaluation and management of patients with coronary artery disease and heart failure. The first section emphasized a new conceptual approach to changes in the diastolic pressure-volume relation of the left ventricle. Although previous studies have concentrated on mathematical models which describe wall stress and stiffness as derived from the pressure-volume relationship, this review emphasizes that hemodynamic factors are very important in acutely altering the pressure-volume relationship of the left ventricle. This is partly due to alterations in right ventricular pressure, which subsequently influence the left ventricular pressure-volume relationship. In addition, recent studies have pointed out that compliance indices measured at low end-diastolic pressures differ from the indices measured at high end-diastolic pressures, so that limited information from one portion of the curve may not be generalized to describe the entire curve. The section on afterload emphasized the importance of this factor in influencing cardiac function, particularly in the presence of heart failure. In patients with both acute and chronic heart failure, vasodilator drugs which reduce ventricular afterload have produced substantial hemodynamic benefit by reducing the filling pressures of the right and left ventricles and increasing forward cardiac output. This hemodynamic improvement in response to afterload reduction is predictable from the different quantitative descriptions of ventricular afterload. Nevertheless, it is still unclear which method best describes afterload. Although wall stress, impedance, vascular resistance, and aortic pressure have all been utilized as a measure of afterload, each has some shortcomings which may limit its applicability. The final section reviewed approaches to the measurement of regionally ischemic myocardium. Since current studies have emphasized the importance of identifying and preserving ischemic, but viable, myocardium, this section has reviewed techniques for measuring local mechanical performance. Previous studies with the Walton-Brodie strain gauge and epicardial length gauge did not appear to be as satisfactory as more recent measurements with ultrasonic crystals, which can simultaneously measure wall thickness and segment length. These methods form the basis for ongoing experiments designed to evaluate approaches for preserving ischemic myocardium in the setting of experimental myocardial infarction.
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PMID:Cardiac dynamics. 32 99

Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.
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PMID:Echocardiography in ischemic heart disease. 32 1

Verapamil, a calcium antagonist, has been used extensively for treatment of cardiac arrhythmias. Concern persists, however, that it may seriously depress myocardial function in cardiac patients. To investigate this possibility, 20 patients with coronary artery disease (CAD) but no heart failure were given intravenous verapamil (0.1 mg/kg bolus, followed by 0.005 mg/kg/min infusion), and studied hemodynamically and angiographically. Verapamil markedly lowered mean aortic pressure (94 +/- 17 to 82 +/- 13 mm Hg, p less than 0.0005) and systemic vascular resistance (1413 +/- 429 to 1069 +/- 235 dyn-sec-cm5, p less than 0.0005). Simultaneously, all indices of left ventricular (LV) performance greatly improved: cardiac index rose from 2.8 +/- 0.6 to 3.1 +/- 0.7 1/min/m2 (p less than 0.0005), mean velocity of circumferential fiber shortening increased from 0.85 +/- 0.39 to 0.97 +/- 0.46 circ/sec (p less than 0.01), and ejection fraction improved from 55 +/- 16 to 61 +/- 18% (p less than 0.01). No significant changes were noted in the heart rate before and after verapamil administration, and verapamil did not worsen the extent of LV asynergy in the majority of patients. In patients with CAD, the intrinsic negative inotropic effect of verapamil is of negligible importance because its potent vasodilatory properties more than compensate for any intrinsic decrease in LV contractility, and thereby improve the overall cardiac function.
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PMID:Effects of verapamil on myocardial performance in coronary disease. 36 90

During a three-year period 10 patients with critical aortic stenosis were referred to a cardiac referral centre with symptoms and signs of intractable cardiac failure and low cardiac output. In nine patients the correct diagnosis was not suspected at the referring hospital, and in the remaining patient the true severity of the aortic stenosis was not appreciated and cardiomyopathy was suggested as an additional diagnosis. The most common referral diagnoses were severe mitral regurgitation (four patients), congestive cardiomyopathy (two patients), or both (three patients). Only two patients had soft ejection systolic murmurs at the base of the heart radiating into the neck, and such a murmur appeared in a third patient during medical treatment. The carotid pulses were of small volume but the characteristic slow-rising, anacrotic nature of the pulse could not be appreciated clinically. The diagnosis was suspected in nine patients because of aortic valve calcification detected by lateral chest x-ray examination in seven patients and by x-ray screening of the heart in two, and because of abnormal aortic valve echoes in the echocardiogram of all five patients in whom the aortic valve could be seen. Eight patients underwent aortic valve replacement despite seemingly poor preoperative left ventricular function. Three patients died, of whom two had severe coexistent coronary artery disease. The five survivors all returned to normal lives and needed little or no medication.Critical aortic stenosis should be actively sought in patients with severe heart failure of unknown cause since surgery may enable them to resume their normal lives.
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PMID:Occult aortic stenosis as cause of intractable heart failure. 43 94

Each day, for one year, the medical records of adult patients who died in hospital were reviewed before seeing the necropsy findings. For those patients who had had chronic left or left and right heart failure, a presumptive cause was assigned on the basis of antemortem clinical data. Of 740 consecutive patients who were studied at necropsy, 90 had had chronic heart failure. In 15 patients the cause of heart failure was not apparent by clinical criteria; of these, 7 were found at necropsy to have cardiomyopathic syndrome caused by coronary artery disease. In retrospect, the presence of overt diabetes mellitus was a clue that cardiomyopathy caused by coronary artery disease was the cause of clinically unexplained heart failure; 5 of 7 patients with unexplained heart failure who were found to have this at necropsy were diabetic, whereas only 1 of the other 8 patients with clinically unexplained heart failure was diabetic (P less than 0.05). Patients in whom clinically unexplained heart failure was found to be the result of cardiomyopathy caused by coronary artery disease had multiple myocardial infarctions on pathological examination, which, with one exception, were nontransmural. By contrast, myocardial infarctions were transmural on pathological examination in each of 7 matched 'controls' with heart failure, in whom the diagnosis of coronary artery disease had been clinically apparent (P less than 0.01).
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PMID:Cardiomyopathic syndrome caused by coronary artery disease. III: Prospective clinicopathological study of its prevalence among patients with clinically unexplained chronic heart failure. 46 32

The effects of intravenous dopamine were evaluated in 10 patients with severe but stable coronary artery disease, 17 consecutive patients with primary cardiogenic shock and 3 with severe congestive heart failure and oliguria. Dopamine infusion at 10 mug/kg.min in the 10 patients increased cardiac output by 35%, left ventricular peak dP/dt by 38%, left ventricular minute work index by 44% and mean systolic ejection rate by 7% (P < 0.01); heart rate, aortic pressure, left ventricular end-diastolic pressure and tension-time index were unchanged. For oxygen, potassium and lactate, arterial and coronary sinus values, coronary arteriovenous oxygen differences and myocardial extraction were unchanged. Hemodynamically 13 of the 17 patients in shock responded favourably to dopamine infusion (0.5 to 15 mug/kg.min), with decrease in heart rate, increase in systolic arterial pressure from 75 to 100 mm Hg (P <0.001), decrease in ventricular filling pressure from 20 to 16 mm Hg (P < 0.01) and increase in urine output from 10 to 100 ml/h (P < 0.01). Eleven of those patients survived the shock episode. A close relation was observed between the hemodynamic response to dopamine, survival from the shock episode and the time between onset of shock and initiation of therapy. Low rates of dopamine infusion induced diuresis in the three patients with severe cardiac failure.Dopamine thus seems to improve the mechanical efficiency of the heart in coronary artery disease. Cardiac output is selectively increased and myocardial ischemia does not appear to be induced; those beneficial effects as well as presumably specific action on renal flow and natriuresis, improve immediate survival from cardiogenic shock and severe heart failure.
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PMID:Hemodynamic and therapeutic effects of intravenous dopamine. 60 65

Overt liver disease caused by left-sided heart failure is seldom recognized unless there is obvious hypotension. We now report 4 patients whose initial diagnosis was hepatitis but who were later shown to have central hepatic necrosis associated with left ventricular failure. Signs of right-sided heart failure were absent. Hepatitis was initially suspected in 3 patients because of striking transaminase elevations and in 1 patient because of jaundice and symptoms compatible with hepatitis. Liver biopsies performed on all patients revealed central hepatic necrosis without evidence of acute or chronic hepatitis. Left ventricular failure was documented in all 4 patients. One patient had coronary artery disease, and the other three patients had valvular heart disease. Liver function tests became normal or improved in all cases as the underlying heart disease was treated. We believe that liver dysfunction secondary to left ventricular failure is not uncommon and can be seen in the absence of right-sided heart failure or hypotension.
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PMID:Left-sided heart failure presenting as hepatitis. 63 89

Left ventricular myocardial stiffness was calculated in clinical cases. Thirty patients who underwent diagnostic cardiac catheterization were studied. Left ventricular cineangiograms and simultaneously recorded left ventricular pressure tracings were analyzed. The left ventricular stiffness constant k, was computed by substituting the left ventricular myocardial stress (sigma) and strain (epsilon) throughout the period between the end of rapid ventricular filling and the beginning of atrial contraction, in the equation sigma = b.ek.epsilon. Left ventricular myocardial stiffness was measured as follows: Group I (normal): 9.6 +/- 4.3, Group II (mitral stenosis): 10.7 +/- 4.0, Group III (left ventricular volume overload): 12.1 +/- 4.2, Group IV (coronary artery disease without myocardial infarction): 8.6 +/- 2.5, and Group V (myocardial infarction): 23.6 +/- 7.4. All of the normal cases showed stiffness constants of less than 15 and maxVcf of more than 2.0 circ/sec, and all the patients with histories of heart failure in Groups III to V showed stiffness constants of more than 15 and maxVcf of less than 1.0 circ/sec. For the rest of the patients, measurements of the stiffness constant were valuable for the assessment of patients' clinical status, especially when combined with contractility.
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PMID:Clinical evaluation of left ventricular myocardial stiffness. 65 Sep 1

Nineteen patients, aged 58-80 years, with severe isolated aortic valve stenosis, severely reduced ejection fraction and clinical heart failure underwent aortic valve replacement between January 1970 and April 1977. Ten had concomitant coronary artery disease (all underwent additional coronary bypass surgery), 17 had angina pectoris and four had syncope. Aortic valve area index was 0.32 +/- 0.03 cm2/m2 (mean +/- SEM); left ventricular (LV) end-diastolic volume index was 117 +/- 9 ml/m2 and LV ejection fraction was 0.37 +/- 0.02. There were four operative deaths and one late death. The follow-up time ranged from six to 74 months (38 +/- 6 months). Actuarially determined three-year survival is 74 +/- 10%; the expected five-year survival is the same. One patient had a serious cerebrovascular accident. Of the remaining survivors, seven were initially Functional Class IV and six Class III; currently, six are Class I and seven Class II (New York Heart Association classifications). The cardiothoracic ratio has decreased from 0.54 +/- 0.03 to 0.49 +/- 0.03. Repeat hemodynamic evaluation has been performed in 10 patients, 22 +/- 6 months after surgery. In these 10 patients, the aortic valve gradient decreased from 55 +/- 7 11 +/- 1.3 mm Hg; LV end-diastolic pressure from 22 +/- 2.4 to 9 +/- 1.9 mm Hg; LV end-diastolic volume index from 119 +/- 16 ml/m2 to 107 +/- 11 ml/m2. LV ejection fraction has increased dramatically from 0.34 +/- 0.03 to 0.63 +/- 0.05 and mean velocity of circumferential fiber shortening from 0.57 +/- 0.08 to 1.3 +/- 0.18 circ/sec. The encouraging long-term survival, improved functional class and the marked improvement in left ventricular function that occurred in our patients indicate that all patients with severe aortic stenosis in clinical heart failure should be offered aortic valve replacement.
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PMID:Severe aortic stenosis with impaired left ventricular function and clinical heart failure: results of valve replacement. 66 73

In order to evaluate the effects of rapid digitalization on LV volumes, ejection fraction, and asynergy, 21 patients without heart failure were studied with a combination of hemodynamic and angiographic techniques before and after administration of intravenous ouabain (0.007 mg./Kg.). Seven patients had no CAD and served as normal (control) subjects (Group I), while 14 patients had extensive coronary disease (Group II). All pre-ouabain parameters were within the normal limits in Group I. After ouabain infusion, all indices of LV contractility: dP/dt, VCF, and ejection fraction rose significantly in the normal group, while LV filling pressure and end-diastolic volume remained unchanged. The baseline hemodynamic and volumetric values for Group II patients corresponded closely to their normal (Group I) counterparts, and exhibited similar changes after ouabain administration. Eight patients in Group II also had regional disorders of LV contractility, delineated by 23 abnormal hemiaxes of shortening. After ouabain, 15 out of 23 asynergic segments (65 per cent) improved, seven remained unchanged, and one worsened. It is therefore concluded that rapid digitalization not only enhances LV performance in normal subjects and in patients with CAD, but can also markedly reduce the extent of LV asynergy.
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PMID:Effects of rapid digitalization on total and regional myocardial performance in patients with coronary artery disease. 68 6


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