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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.
Am J Cardiol 1976 Mar 31
PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

Hemodynamics and myocardial contractility were evaluated in five unanesthetized calves during acute hypocapnic and isocapnic hypoxia and during acute hypocapnic hypoxia with beta-adrenergic blockade. Both hypocapnic and isocapnic hypoxia, with mean PaO2 levels of 33.1 and 39.1 mm Hg respectively, produced a decline in stroke volume and index, while cardiac output and index were maintained at normoxic control levels by an increase in heart rate. Evaluation of myocardial contractility indices suggested an augmentation of left ventricular contractility during both hypocapnic and isocapnic hypoxia. Beta-adrenergic blockade effectively eliminated the increase in left ventricular contractility during hypocapnic hypoxia, suggesting an important role of the adrenergic nervous system in the genesis of the cardiovascular response of the calf to acute hypoxia. Right ventricular contractility indices failed to demonstrate a clear-cut augmentation of contractility during hypocapnic and isocapnic hypoxia when the concurrent increase in afterload was considered. Mean pulmonary arterial blood pressure rose significantly during hypocapnic and isocapnic hypoxia. The pulmonary pressor response to hypocapnic hypoxia was significantly augmented by beta blockade, indicating that the autonomic nervous system is capable of modifying the hypoxic pulmonary pressor response in this species.
Basic Res Cardiol
PMID:Myocardial function during acute hypoxia in the calf. 1 80

Studies of cardiac hypertrophy in spontaneously hypertensive rats have indicated that left ventricular hypertrophy occurred even in the prehypertensive stage. These findings suggested that other factors besides blood pressure levels, and including possibly a genetic predisposition to myocardial hypertrophy, could play a role in structural cardiovascular alterations in spontaneously hypertensive rats. More recent studies have confirmed these anatomic results; left ventricular hypertrophy was vectorcardiographically detected even in the prehypertensive stage in voth young stroke-prone rats and stroke-resistant spontaneously hypertensive rats. Further, a close relation was found between degree of left ventricular hypertrophy and vascular hypertrophy or hyperplasia; this suggests that early detection of left ventricular hypertrophy may be a useful indicator of the incipient stage of structural vascular changes in genetic hypertension.
Am J Cardiol 1979 Oct 22
PMID:Cardiac hypertrophy in early hypertension. 4 Apr 30

To determine the prognosis for the newborn with transposition of the great arteries, the clinical course of 112 consecutive neonates with dextrotransposition was reviewed. Patients were managed with balloon atrial septostomy at initial cardiac catheterization, palliative operation if needed in the 1st year of life and Mustard's intraatrial baffle repair. The 1st month of life was the period of greatest risk (8 percent mortality rate). Between balloon septostomy and baffle repair, 14 of 103 patients at risk (14 percent) either died or had a cerebrovascular accident. The mortality rate at baffle repair was 14 percent (10 deaths in 71 patients), and there were 3 late postoperative deaths. Actuarial analysis of the data indicates that with this plan of management, approximately 50 percent of newborns with transposition of the great arteries will survive 5 years with excellent function and an additional 15 to 20 percent will survive with one or more medical handicaps.
Am J Cardiol 1979 Jul
PMID:Prognosis for the newborn with transposition of the great arteries. 8 73

It has been shown that hydralazine is beneficial in chronic heart failure by virtue of its afterload reducing effect. Nitroglycerin paste results in venodilation and fall in left ventricular filling pressure (LVFP). Thirteen patients with chronic heart failure were given a combination of oral hydralazine and nitroglycerin paste. With oral hydralazine (75 to 100 mg every 8 h), left ventricular stroke work increased and LVFP slightly fell. Following addition of 2% nitroglycerin paste, an additional decline in mean pulmonary artery and LVFP was observed without significant changes in heart rate and arterial pressure. There were no untoward side effects from either therapy. Eight patients followed for three to eight months (mean five months) reported subjective improvement in shortness of breath and other symptoms related to ventricular dysfunction. This study shows that in certain patients with chronic heart failure, hydralazine and nitroglycerin paste combination produces salutary clinical effects on long term probably through afterload and preload reduction, respectively.
Clin Cardiol 1978 Aug
PMID:Non-parenteral combined afterload and preload reduction therapy in congestive heart failure. 11 91

The hemodinamic effects of Amrinone, bipiridine derivate with positive inotropic effects in animals, were studied on eight patients under right and left heart catheterization. The cardiac index, stroke volume, dP/dt and stroke work index were increased; the pulmonary pressure and the left ventricle end diastolic pressure were decreased all with statistical significant values. There were no changes in mean aortic pressure. These effects are mainly due to an increase in contractility and, partially, to vasodilation and tachycardia. The intrinsic mechanism of action of this compound is not known. Its place in cardiac therapy must be established with additional clinical investigations.
Arch Inst Cardiol Mex
PMID:[Hemodynamic effects of various doses of a new inotropic: amrinoma]. 12 81

Hemodynamic and electrophysiologic studies were performed in 11 children with dextrotransposition of the great arteries an average of 26 months after the interatrial baffle procedure and, in 2 patients, additional closure of a ventricular septal defect. All children are clinically well. Right to left shunts ranging from 28 to 63 percent of systemic blood flow were found at the superior vena caval-baffle junction in four children. The superior vena caval-baffle gradient averaged 7 mm Hg (range 0 to 22). Right ventricular stroke work index averaged 39 g-m/beat per m2 and right ventricular end-diastolic pressure 9 mm Hg. These values were not significantly different from the values for the systemic left ventricle in a comparable group of normal children (average left ventricular stroke work index 45 g-m/beat per m2 and average left ventricular end-diastolic pressure 8 mm Hg). Cardiac index, heart rate and arteriovenous oxygen difference were also normal. No child has complete heart block. His bundle recording demonstrated normal H-V intervals (range 27 to 40 msec); 4 of the 11 had a prolonged A-H interval. Left ventricular systolic pressure was less than 40 mm Hg in all but two children who had significant subpulmonary stenosis. Pulmonary vascular resistance averaged 1.9 units and was decreased in all children. We conclude that up to 37 months postoperatively, despite some residual abnormalities, the clinical and hemodynamic condition of these children is excellent.
Am J Cardiol 1975 May
PMID:Postoperative hemodynamic and electrophysiologic evaluation of the interatrial baffle procedure. 12 1

Six patients with aortic root dissection proved by angiography, surgery or autopsy, and six patients with aortic root dilatation were studied by echocardiography. Echocardiography was diagnostic in five or six patients with dissection and suggestive in the sixth, disclosing anterior and posterior dissection in three, anterior dissection in one and posterior dissection in one. The recording of a double echo in the aorta was the diagnostic feature. Angiography was diagnostic in four of the six patients, yielded a false negative result in one and was not performed in one. Six patients with dilatation had an enlarged aortic root by echocardiography. Left ventricular size, stroke volume, ejection fraction, aortic regurgitant flow and velocity of circumferential fiber shortening were calculated in 11 patients. Echocardiography was extremely helpful in the diagnosis, management and follow-up in patients with aortic dissection or dilatation.
Am J Cardiol 1975 Jul
PMID:Echocardiography in aortic root dissection and dilatation. 12 34

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
Am J Cardiol 1976 Nov 23
PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

Evaluation of left ventricular performance in aortic stenosis, aortic regurgitation and mitral regurgitation from the stroke work/left ventricular mass ratio. Europ. J. Cardiol., 10/4, 279--294. 132 patients with a pure valvular dysfunction affecting a single orifice, namely aortic stenosis, aortic or mitral regurgitation, were studied. All patients, including 20 control subjects, underwent hemodynamic examination of both right and left heart chambers including left cineangiography. Using the stroke work index/myocardial mass ratio (SWI/MLV), for which the limits in normal subjects are narrow (0.81 +/- 0.03 . g-1) it was possible to divide these patients into three groups: Group I (SWI/MLV greater than 0.87 gm . g-1) characterized by a proportionately greater increase in stroke work index than myocardial mass (hyperfunctioning ventricle). Group II (0.87 gm . g-1 greater than or equal to SWI/MLV greater than or equal to 0.75 gm . g-1) characterized by a parallel increase in stroke work index and myocardial mass (normally functioning ventricle). Group III (SWI/MLV less than 0.75 gm . g-1) for which the increase in myocardial mass was proportionately greater than that of the stroke work index (hypofunctioning ventricle). As one progresses from group I to III, there is a concomitant fall in ventricular function with decreased mean velocity of circumferential fiber shortening (VCF), ejection fraction (EF) and increased enddiastolic volume (EDV) together with the hypertrophy of the left ventricle during the last stage. We conclude that the SWI/MLV ratio is an easy to calculate index, independent of the unerlying dysfunction, which evaluates left ventricular function by taking into account the myocardial mass.
Eur J Cardiol 1979 Oct
PMID:Evaluation of left ventricular performance in aortic stenosis, aortic regurgitation and mitral regurgitation from the stroke work/left ventricular mass ratio. 15 81


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