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

The mitral apparatus is a complex structure composed of several components, each of which can be affected by a variety of diseases, resulting in mitral regurgitation. The physiologic consequences of mitral regurgitation include reduced forward stroke volume; increased left atrial volume and pressure; and reduced resistance to left ventricular ejection. The latter explains why indices of systolic left ventricular function (ejection fraction) are often increased early in the course of mitral regurgitation. With the insidious development of mitral regurgitation, the left atrium dilates to accommodate the increase in volume, thereby reducing the atrial pressure. However, with the acute development of mitral regurgitation into a nondilated left atrium, pressure rises rapidly, producing pulmonary edema. The predominant clinical symptoms in chronic mitral regurgitation of dyspnea and fatigue result from pulmonary venous hypertension and low cardiac output. The cardinal physical finding is a mitral systolic murmur. Since the murmur can assume various configurations, the most reliable way to establish its correct origin is by bedside physiologic maneuvers. Typically, in the beat following a premature contraction or after a long pause during atrial fibrillation, the murmur of mitral regurgitation is unchanged in intensity, but murmurs due to left ventricular outflow obstruction increase. Also, isometric handgrip exercise increases the intensity of the murmur and a Valsalva maneuver decreases it during the strain phase. Echocardiography is the most useful noninvasive technique for evaluating patients with mitral regurgitation. Visualization of the mitral apparatus may establish the etiology of regurgitation, and measurement of left atrial size and left ventricular size and performance is useful for assessing the functional significance of the lesion. Doppler echocardiography can establish the diagnosis of mitral regurgitation in difficult cases with multi valve disease and can estimate the severity of the regurgitation. Cardiac catheterization and angiography are usually reserved for the patient being considered for valvular surgery. The natural history of chronic mitral regurgitation is characterized by slowly progressive symptoms, and often the onset of disabling symptoms is the result of irreversible left ventricular dysfunction. Medical therapy consists of digitalis, diuretics, and vasodilators for symptomatic patients. When symptoms occur despite this therapy, valvular surgery should be considered before left ventricular function becomes abnormal.
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PMID:Mitral valve regurgitation. 637 82

Ten minutes of cerebral ischemia was produced in 12 dogs by temporary ligation of the venae cavae and aorta. After reperfusion the dogs received the calcium entry blocker, flunarizine, 6 micrograms/kg infused over a ten minute period. Cerebral blood flow (CBF) and metabolism (CMRO2) were measured pre-ischemia and for 2 h post-ischemia in 6 dogs. At the end of the study brain biopsies were analyzed for cerebral metabolites. Neurologic recovery was evaluated for up to 48 h post-ischemia in an additional 6 dogs. The results of each study were compared to those previously obtained in untreated animals. The cerebral blood flows (when expressed as a percent of the pre-ischemic control value) of the flunarizine-treated and untreated groups were similar throughout the post-ischemic period. Following an initial hyperemia, the CBF fell to significantly less than the pre-ischemic control values, and remained approximately 26% of control during the final 90 min in both groups. The CMRO2 was also the same for both groups. Cerebral metabolites were similar although abnormal in both groups. Flunarizine produced pulmonary edema in 5 of 6 dogs studied for neurologic recovery. Four of these dogs died within 12 h and another dog demonstrated severe neurologic damage. None of the untreated dogs developed pulmonary edema, but 6 of 7 dogs evidenced severe neurologic damage or were dead at 48 h. Thus, flunarizine failed to improve either cerebral blood flow or neurologic outcome when given after complete cerebral ischemia in the dog. A cardiodepressive effect of flunarizine might have contributed to the poor neurologic outcome.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke
PMID:Failure of flunarizine to improve cerebral blood flow or neurologic recovery in a canine model of complete cerebral ischemia. 646 59

Thirty-two consecutive patients with acute myocardial infarction (AMI) were studied during the first seven days following AMI. The stroke volume was measured by impedance cardiography. The patients were divided into two groups: Group A (n = 22), with clinically uncomplicated myocardial infarction and Group B (n = 10) with evidence of congestive failure, but not of pulmonary edema. Patients in Group B had predominantly anterior wall myocardial infarction compared to Group A (p less than 0.05). The heart rate was significantly greater in Group B compared to Group A (p = 0.0002). The systolic blood pressure, the mean blood pressure, stroke volume index, and left ventricular stroke work index were significantly lower (p less than 0.05) in Group B than Group A. Impedance cardiography can be easily applied to follow the course of the patients during the acute phase of myocardial infarction.
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PMID:Hemodynamics in acute myocardial infarction the use of impedance cardiography. 658 97

Hyperbaric oxygenation (HBO) was included in the therapeutic complex for 124 patients in the acute stage of ischemic stroke. The effect of HBO on the clinical course was appraised by comparing the dynamics of changes in the clinical symptoms and the frequency of complications in patients exposed to HBO with those in the control group (patients not exposed to HBO). It was established that the depth of unconsciousness and the motor and aphasic disorders decreased during a HBO session, but the effect was usually short-lived. Aggravation of the patients' condition in the first week of the disease, evidently caused by increase of cerebral edema, occurred much less frequently when HBO was included in the complex of therapeutic measures. The number of patients with regression of the neurological symptoms was practically the same with and without the use of HBO, but the regression of the neurological defects was most evident in patients exposed to HBO. HBO prevents the development of recurrent cerebral circulatory disorders in the acute stage of ischemic stroke and reduces the incidence of some complications in this period (pneumonia, pulmonary edema, thromboembolism of the pulmonary artery, etc.).
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PMID:[Effect of hyperbaric oxygenation on the clinical course and complications of the acute period of ischemic strokes]. 661 31

The haemodynamic effects of intravenous frusemide (1 mg/kg) were studied in 22 male patients with left ventricular failure following acute myocardial infarction. Radiographic pulmonary oedema was present in all patients and their average left heart filling pressure was 20 mmHg. Bolus injection of the drug was followed by immediate increases in systemic arterial pressure (P less than 0.05) and heart rate (less than 0.05); these declined to pre-injection values after 60 min. Following frusemide there were progressive reductions in left heart filling pressure (P less than 0.01), thermodilution cardiac output (P less than 0.01) and stroke volume (P less than 0.05) and a progressive increase in the derived systemic vascular resistance (P less than 0.05). There was an average diuresis of 860 ml during the 90 min following the frusemide injection. The influence of frusemide on left ventricular performance was studied by comparing the circulatory effects of passive leg raising in the control period with those at 30, 60 and 90 min after the drug. In the control period this manoeuvre increased left heart filling pressure, but not heart rate, cardiac output, stroke volume or systemic vascular resistance. Ninety minutes after frusemide, but not before, passive leg raising resulted in a significant increase in cardiac output (P less than 0.01) and stroke volume at a similar increment in filling pressure and a significant reduction in the systemic vascular resistance (P less than 0.05). These circulatory actions of intravenous frusemide are compatible with initial arteriolar constriction and venodilatation followed by depletion of blood volume with subsequent change in left ventricular pumping performance.
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PMID:Haemodynamic effects of frusemide and its influence on repetitive rapid volume loading in acute myocardial infarction. 665 80

Twelve patients with acute myocardial infarction and radiological evidence of pulmonary oedema were observed in whom the left atrial pressure, measured indirectly as pulmonary artery end-diastolic pressure, was not critically increased (range 5-12 mm Hg with reference to sternal angle). Eight of the patients had been treated with frusemide, but only six had responded: hence in at least half of the series diuresis could not account for the anomalous finding. Six patients with low cardiac output were given infusions to expand plasma volume. Appreciable increments in mean values for cardiac index (1.6 to 2.0 1/min/m2), stroke index (18 to 23 ml/beat/m2), mean arterial pressure (65 to 86 mm Hg), and pulmonary artery end-diastolic pressure (8 to 15 mm Hg) were recorded. This group, and the remaining six patients with higher cardiac output, survived to leave hospital. Delay in radiographic clearing after a fall of left atrial pressure was a possible explanation for the relatively low pulmonary artery end-diastolic pressures, especially in the patients treated successfully with diuretics. Other mechanisms, such as alterations in pulmonary vascular permeability, might also have contributed to the syndrome. Pulmonary oedema without a critical increase in the left atrial pressure is unusual in acute myocardial infarction but the therapeutic implications are important. Withdrawal;of diuretics may be indicated, and in some cases expansion of plasma volume may lead to striking clinical improvement.
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PMID:Pulmonary oedema without critical increase in left atrial pressure in acute myocardial infarction. 679 Jan 11

We measured the clearance from blood to pulmonary edema fluid of a small molecular weight hydrophilic radiotracer, Indium-111-DTPA (In-DTPA) and a larger molecular weight radiotracer, Iodine-125-HSA (I-HSA), in patients with pulmonary edema on either a cardiac or noncardiac (permeability) basis. In previous investigations, we had noted an apparent relationship between the magnitude of clearance of I-HSA across the alveolocapillary membrane and the severity of noncardiac pulmonary edema. In this study, we were able to distinguish at least 2 distinct groups of patients with noncardiac pulmonary edema. Patients with the greatest damage to the alveolo-capillary exchanging membrane, defined by the flux of I-HSA from blood to edema fluid, were significantly differentiated from those with a lesser microvascular injury on the basis of higher mean heart rate (HR), temperature, cardiac index (CI), pulmonary artery pressures, right ventricular stroke work index (RVSWI), and a lower mean total white blood cell count (WBC), among others. Therefore, noncardiac pulmonary edema is characterized by a spectrum of permeability injury to the pulmonary microvasculature which seems to parallel other measurable indices of the severity of the systemic response to the illness.
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PMID:Clinical correlates of the spectrum of lung microvascular injury in human noncardiac edema. 682 83

The aim of the present study was to determine whether induction of ischaemic heart failure by micro-embolization leads to only a single episode of myocardial injury or whether it sets up a vicious cycle of progressive myocardial damage. Acute left ventricular (LV) failure was produced in 15 closed-chest anaesthetized dogs by injection of 50 microns plastic microspheres into the left main coronary artery. The dogs showed signs of severely depressed LV function; there was a marked increase in LV end-diastolic pressure and a marked decrease in stroke volume. Myocardial lactate uptake decreased or reversed to production. Six dogs with very high LV end-diastolic pressure died during the subsequent 3 days and autopsy revealed pulmonary edema. The LV function was re-examined in four dogs at 2 and 4 weeks after embolization. Except for a modest elevation of LV end-diastolic pressure there were no haemodynamic or metabolic signs of myocardial dysfunction. Gross and light microscopic examination of the heart in dogs 8 hours to 6 weeks following microsphere injections revealed numerous small infarcts or focal areas of granulation or scar tissue throughout the entire left ventricle. At 1 to 6 weeks close to the infarcts there were scattered myocytes with strong eosinophilia and pyknosis or loss of nuclei, interpreted as myocytolysis. In two dogs killed at six weeks after the embolization there were areas of granulation tissue, similar to a recent infarction about 1 week old. Thus, in spite of apparent functional restoration there were morphological signs of repeated and progressive myocardial injury several weeks after coronary embolization.
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PMID:Progression of myocardial damage following coronary microembolization in dogs. 684 15

To assess the prognostic importance of resting left ventricular function in survivors of acute myocardial infarction with pulmonary edema, we retrospectively identified 39 consecutive patients who presented with acute pulmonary edema and myocardial infarction. Sixteen patients had radionuclide ejection fractions 10 +/- 2 days postinfarction of greater than 0.45 (group A, mean 0.55 +/- 0.06), and 23 patients had ejection fractions less than or equal to 0.45 (group B, 0.32 +/- 0.06). There were no significant differences between the two groups for age or sex, but group A patients had a significantly greater incidence of first myocardial infarction predominantly inferior in location. The calculated stroke work index during the acute event was significantly greater in group A than in group B (33.4 +/- 2.4 vs 23.4 +/- 2.0) (p less than 0.05). During a follow-up of 9 +/- 3 months, mortality was not significantly different between the two groups: Four (25%) died in group A and seven (30%) died in group B. In addition, eight patients (50%) in group A were hospitalized for recurrent angina, new myocardial infarction or recurrent pulmonary edema, compared with 11 (48%) in group B (NS). Three deaths in group A were preceded by infarction of the anterior wall of the left ventricle, confirmed at autopsy, and two nonfatal infarctions were anterior by electrocardiography. Four patients in group A had coronary arteriography performed during the follow-up period because of unstable angina, and all had significant (greater than or equal to 70% stenosis) three-vessel disease and two had left main coronary artery disease. Therefore, the predischarge ejection fraction did not predict prognosis for this group of patients. Patients with acute pulmonary edema in the course of myocardial infarction form a high-risk group despite good resting left ventricular function at discharge. They have a significant incidence of recurrent myocardial infarction and death and, because they have good residual left ventricular function, are excellent candidates for surgical intervention.
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PMID:Prognosis of patients with acute pulmonary edema and normal ejection fraction after acute myocardial infarction. 684 21

Tumoricidal reactions in dogs with spontaneous breast carcinoma occur after perfusion of plasma over protein A derived from Staphylococcus aureus and immobilized in collodion charcoal. When this treatment was extended to humans with breast cancer, hemodynamic and physiologic changes were noted. The evolution and spectrum of these reactions were evaluated during 47 plasma infusions in five patients. Initial treatment conditions consisting of rapid perfusion of plasma over high quantities of immobilized protein A were employed for 12 treatments in two patients. Within 30 minutes after treatments were begun, mean blood pressure, systemic vascular resistance, and stroke volume increased, as did heart rate, cardiac output, and rectal temperature; however, mean pulmonary artery pressure and total pulmonary resistance did not change. At 90 minutes, hypotension developed (lowest mean blood pressure was 59 +/- 14 mm Hg) that was associated with a decrease in systemic vascular resistance and total pulmonary resistance (536 +/- 66 and 146 +/- 44 dynes . second . cm-5, respectively). Cardiac output increased, tachycardia developed, stroke volume decreased, and rectal temperature increased. During the hypotensive phase, values of creatinine clearance and fractional excretion of sodium diminished. Noncardiogenic pulmonary edema appeared occasionally, with bronchospasm noted once. No hemodynamic changes were seen when saline solution was passaged over protein A immobilized in collodion charcoal or when autologous plasma was given without passage over protein A immobilized in collodion charcoal. Treatment conditions were modified by diminishing protein A quantity and plasma volume and slowing plasma perfusion rate, which resulted in significant attenuation of all cardiopulmonary responses. This report, then, defines for the first time the physiologic basis of the cardiopulmonary toxicity in humans after plasma perfusion over immobilized protein A.
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PMID:Cardiopulmonary toxicity in patients with breast carcinoma during plasma perfusion over immobilized protein A. Pathophysiology of reaction and attenuating methods. 688 Nov 80


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