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

Indexes of left ventricular diastolic filling were measured by pulsed Doppler echocardiography in 21 insulin-dependent diabetic patients and 21 control subjects without clinical evidence of heart disease. No patient had chest pain or electrocardiographic changes during exercise testing. The mean age of patients was 32 years. All patients had a normal ejection fraction. Six (29%) of the 21 diabetic patients had evidence of diastolic dysfunction as assessed by the presence of at least two abnormal variables of mitral inflow velocity. The ratio of peak early to peak late (atrial) filling velocity was significantly decreased in diabetic compared with control subjects (1.24 +/- 0.21 versus 1.66 +/- 0.30, p. less than 0.001). Atrial filling velocity was significantly increased in diabetic patients (74.3 +/- 16.7 versus 60.3 +/- 12.2 cm/s, p less than 0.004), whereas early filling velocity was reduced by a nearly significant degree (88.8 +/- 12.6 versus 98.5 +/- 18.8 cm/s, p less than 0.057). The atrial contribution to stroke volume as assessed by area under the late diastolic filling envelope compared to total diastolic area was also significantly increased in diabetic compared with control subjects (35 versus 27%, p less than 0.001). Left ventricular diastolic filling abnormalities in diabetic patients did not correlate with duration of diabetes, retinopathy, nephropathy or peripheral neuropathy. These data suggest that approximately one-third of such patients have subclinical myocardial dysfunction unrelated to accelerated atherosclerosis. Doppler echocardiography may offer a reliable noninvasive means to assess diastolic function and to follow up diabetic patients serially for any deterioration in cardiac status before the appearance of clinical symptoms.
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PMID:Diastolic abnormalities in young asymptomatic diabetic patients assessed by pulsed Doppler echocardiography. 337 97

The term "penetrating aortic ulcer" refers to an ulceration of an atheromatous plaque that extends deeply through the intima and into the aortic media. It may precipitate an intramedial dissection (usually localized) or may rupture into the adventitia to form a pseudoaneurysm. The typical patient with penetrating atheromatous aortic ulcer is elderly and has hypertension, atherosclerosis, and back or chest pain, but pulse deficit, stroke, aortic insufficiency, and compromise of a visceral vessel are not present. Classic aortic dissection and symptomatic thoracic aortic aneurysms are among possibilities in the differential diagnosis. Aortography demonstrates the presence of an aortic ulcer similar in appearance to gastric ulcers seen on barium examination; in addition, an intramural aortic hematoma may be present. Our experience with penetrating aortic ulcers in symptomatic patients indicates that conservative medical therapy leads to recurrence of symptoms and a need for surgical intervention. We present a case that illustrates the salient features of this distinct clinical entity.
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PMID:The penetrating aortic ulcer: pathologic manifestations, diagnosis, and management. 338 11

Since oral contraceptives (OCs) are the method chosen by an estimated 10 million US women, health care providers must be informed about the pill's mechanism of action, its warning signs and contraindications, and its interaction with other drugs and vitamins. Although nearly 60 OC brands are currently available, there are only 2 basic types: the mini-pill, which contains progesterone only, and the combination OC, which adds estrogen. Combination OCs are further divided into monophasic, biphasic, and triphasic preparations. OC use is contraindicated in women with a history of phlebitis, stroke, coronary artery disease, liver tumors, or breast cancer. Warning signs that patients should be instructed to report include acute abdominal pain, chest pain, headaches, and severe leg pain. The effectiveness of OCs is decreased by drugs such as ampicillin, penicillin V, tetracycline, rifampin, barbiturates, and some antiepileptics. On the other hand, OCs decrease the effects of insulin and oral hypoglycemics, oral anticoagulants, and guanethidine. In addition, OCs can increase the risk of certain nutritional deficiencies, primarily of folic acid and vitamins C, B2, B6, and B12.
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PMID:The pill, the patient, and you. 338 42

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.
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PMID:Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia. 339 67

Although myocardial revascularization relieves anginal symptoms, the effect on ventricular function remains controversial. Sixty-six patients undergoing elective coronary bypass surgery with normal right and left ventricular function were studied 1 month preoperatively (PRE), 3-5 hours perioperatively (PERI) and 3-5 months postoperatively (POST). Nuclear ventriculograms were employed to calculate right and left ventricular ejection fractions (RVEF, LVEF), end diastolic volume indices (RVEDVI, LVEDVI) and end systolic volume indices (RVESVI, LVESVI). Cardiac index (CI), stroke index (SI) and an approximation of left ventricular stroke work index (LVSWI) were also calculated from the scintigraphic data. Right and left ventricular ejection fractions were lower perioperatively (PRE:RVEF 37 +/- 2.5, LVEF 61 +/- 3; PERI:RVEF 32 +/- 3, LVEF 51 +/- 4; POST:RVEF 35 +/- 3, LVEF 56 +/- 4%, p less than 0.01 by analysis of variance, ANOVA) despite lower end diastolic volume indices perioperatively, (p less than 0.05 by ANOVA). The ratio of systolic blood pressure to LVESVI was significantly lower PERI than PRE or POST, (p less than 0.01 by ANOVA). SI, LVSWI, LVEF and RVEF were lower perioperatively at any level of LVEDVI or RVEDVI (p less than 0.01 by paired analyses of covariance), suggesting transient depression of right and left ventricular performance perioperatively. Right ventricular recovery was incomplete 4 months postoperatively. The patients were able to exercise longer at higher workloads postoperatively (p less than 0.01 by ANOVA). Chest pain resulted in discontinuation of exercise in 57% of patients PRE but only 5% POST (p less than 0.01), even though all patients were receiving full medical therapy preoperatively and no therapy postoperatively. Myocardial revascularization provided symptomatic relief and increased work capacity. However, right and left ventricular function were transiently depressed in the early perioperative period.
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PMID:Transient biventricular dysfunction following coronary bypass surgery with potassium cardioplegia. 349 45

It is demonstrated that right ventricular volumes can be measured accurately by biplane cineangiography using the Simpson's rule or various area-length methods. In order to validate the single plane approach a biplane (30 degrees RAO-60 degrees LAO) right ventricle (RV) cineangiography was performed in 10 adults investigated for chest pain without coronary artery disease or any other heart disease. RV volumes (EDV: end-diastolic; ESV: end-systolic; SV: stroke volume) and EF (ejection fraction) were measured by biplane and single plane analysis with the same area-length method using the pyramide with triangular base as geometric model (Ferlinz). The results are: RVEDV (ml/m2) biplane (B) 81 +/- 10, monoplane (M) 82 +/- 11; RVESV (ml/m2) B 33 +/- 6, M 35 +/- 8; RVSV (ml/m2) B 48 +/- 8, M 47 +/- 10; RVEF (%) B 59 +/- 6, M 57 +/- 8. Equations of linear regression show the following correlations: RVEDV R = 0.82 p less than 0.01; RVESV R = 0.77 p less than 0.01; RVSV R = 0.92 p less than 0.001; RVEF R = 0.85 p less than 0.01. Authors conclude to a good enough correlation between monoplane and biplane analysis especially for RVSV and RVEF. They underline the great variability of individual values.
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PMID:[Measurement of right ventricular volume by cineangiography. Validation of monoplane analysis compared with biplane]. 361 5

The mechanism of the antianginal actions of nilvadipine was investigated in 11 patients with effort angina pectoris. Hemodynamic data were obtained by angina-limited supine multistage bicycle ergometer exercise testing before and after a single 6 mg dose of nilvadipine. Compared with chest pain during control exercise testing, pain at peak exercise disappeared or abated and the ST segment at peak exercise also showed less significant depression after administration of nilvadipine. At rest and at peak exercise, mean blood pressure, pulmonary artery wedge pressure and systemic vascular resistance decreased significantly, whereas heart rate and cardiac index increased significantly after nilvadipine. Rate-pressure product and stroke volume index did not change significantly. Coronary sinus flow at peak exercise increased significantly and total coronary vascular resistance at rest and at peak exercise decreased significantly after nilvadipine. The plasma concentrations of nilvadipine 1.5 hours after administration ranged from 1.15 to 8.23 ng/ml. These data suggest that the principal factors in the antianginal actions of nilvadipine are an increase in myocardial oxygen supply due to increased coronary blood flow and a reduction in myocardial oxygen demand mainly by a decrease in afterload and additionally by a decrease in preload.
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PMID:Effects of a new second generation calcium channel blocker, nilvadipine (FR34235), on exercise-induced hemodynamic changes in stable angina pectoris. 365 50

Hypertrophic cardiomyopathy (HCM) generally shows increased systolic function of the left ventricle at rest, although patients with HCM often have decreased exercise tolerance and develop dyspnea or chest pain. The present study was to investigate of left ventricular (LV) function during exercise in 26 patients with HCM using Tc-99m equilibrium angiocardiography, and to elucidate the mechanism of impaired functional reserve during exercise. Controls consisted of 11 normal volunteers and 12 patients with chest pain syndrome who had no abnormality on coronary arteriography or left ventriculography. In patients with HCM, LV ejection fraction decreased from 65 +/- 8 (mean +/- SD)% at rest to 59 +/- 18% at peak exercise, in contrast to an increase among controls (from 56 +/- 9% to 64 +/- 9%). As compared with resting values, cardiac output increased to 168 +/- 24% at peak exercise in HCM, but the increase was significantly less than that in controls (215 +/- 47%). Stroke volume decreased gradually to 83 +/- 16% during exercise in HCM, while it increased to 114 +/- 10% at an exercise level of half intensity, and it decreased slightly to 106 +/- 16% at peak exercise. LV end-systolic volume decreased among controls to 78 +/- 27% at peak exercise, but remained unchanged in HCM (118 +/- 58%). An increase in peak ejection rate at peak exercise was less in HCM than in controls (143 +/- 26% vs 170 +/- 42%). No significant differences were observed between the two groups concerning changes in indices of LV diastolic function including LV end-diastolic volume, peak filling rate or 1/3 filling rate during exercise. In the analysis of LV function curves, pulmonary arterial diastolic pressure increased to a greater extent in HCM than in controls (19 +/- 6 mmHg vs 11 +/- 6 mmHg); whereas, an increase in the stroke work index was less in HCM (80 +/- 26 g.m/m2/beat vs 121 +/- 21 g.m/m2/beat) at peak exercise. Thus, the LV function curve shifted downward and to the right in patients with HCM. The above findings indicate that LV functional reserve during exercise is impaired, especially as to systolic function in patients with HCM, while deterioration of diastolic function may be partly compromised by elevated filling pressure.
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PMID:[Left ventricular function in hypertrophic cardiomyopathy: a Tc-99m radionuclide angiographic study during exercise]. 372 81

The interaction between nifedipine and propranolol on cardiac hemodynamics and function was investigated in 9 patients with normal left ventricular (LV) function who were undergoing cardiac catheterization for complaints of chest pain. Only 2 patients had angiographic evidence of significant coronary artery disease but no patient had clinical evidence of ischemia during the study. All patients were pre-treated with propranolol, 30 to 320 mg/day (mean +/- standard deviation 210 +/- 122); the propranolol serum level ranged from 43 to 246 ng/ml (mean 203 +/- 62). The administration of nifedipine resulted in a decrease in blood pressure (from 94 +/- 11 to 85 +/- 13 mm Hg, p less than 0.05), increase in heart rate (from 59 +/- 6 to 65 +/- 7 beats/min, p less than 0.05), and an increase in both mean right atrial and mean pulmonary artery wedge pressures (from 8 +/- 3 to 9 +/- 3 mm Hg and from 13 +/- 3 to 14 +/- 4 mm Hg, respectively, both p less than 0.05). Cardiac index increased (from 2.3 +/- 0.3 to 2.7 +/- 0.2 liters/min/m2, p less than 0.01). Stroke volume index also increased significantly (from 39 +/- 5 to 43 +/- 6 ml/m2) and systemic vascular resistance decreased (from 1,715 +/- 369 to 1,255 +/- 271 dynes s cm-5, p less than 0.01). No significant change was noted in pulmonary vascular resistance (148 +/- 94 vs 140 +/- 62 dynes s cm-5), LV stroke work index (44 +/- 9 vs 42 +/- 10 g-m/m2), LV end-diastolic pressure (15 +/- 2 vs 16 +/- 2 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of nifedipine on hemodynamics and cardiac function in patients with normal left ventricular ejection fraction already treated with propranolol. 375 17

Fourteen patients with acute myocardial infarction (duration of chest pain 5 +/- 2 hours) received intracoronary infusion of prostaglandin E1 (PGE1) and streptokinase. Intracoronary PGE1 was followed by intracoronary streptokinase in 10 patients (group A), with successful recanalization in all patients. Of 4 patients in whom recanalization failed with intracoronary streptokinase given first (group B), 2 had successful recanalization after addition of intracoronary PGE1. Immediately after successful recanalization, left ventricular ejection fraction increased from 50 +/- 9% to 62 +/- 10% (p less than 0.0008), left ventricular end-diastolic pressure decreased from 20 +/- 10 to 16 +/- 10 mm Hg (p less than 0.05) and stroke volume index increased from 34 +/- 10 to 44 +/- 12 ml/m2 (p less than 0.02). Infarct segment shortening improved from 9 +/- 5 to 18 +/- 4% (p less than 0.0002). Transient hypotension in 1 patient was the only complication. Follow-up catheterization in recanalized patients at 2 to 10 days showed maintained improvement in left ventricular global and infarct segment function. Reocclusion occurred in 1 patient. Thus, intracoronary infusion of PGE1 was effective in establishing reperfusion in all patients when followed by streptokinase and was associated with immediately improved left ventricular global and regional function. PGE1 deserves further evaluation in acute myocardial infarction.
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PMID:Intracoronary prostaglandin E1 plus streptokinase in acute myocardial infarction. 378 2


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