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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systolic cusp separation of normal aortic valves has been shown by echocardiography and by angiography to be related to left ventricular stroke volume. In this study, stroke volume was compared with echocardiographic area between the aortic cusps in systole (aortic ejection area). An excellent correlation was observed (r = 0.93) over a wide range of stroke volumes, even in the presence of mitral regurgitation. Stroke volume appears to correlate more closely with aortic ejection area than with angiographic or echocardiographic measurements of peak systolic cusp separation.
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PMID:Echocardiographic aortic ejection area as a reflection of left ventricular stroke volume. 11 43

Isolated mitral insufficiency in children is quantitated angiographically by comparing the stroke volumes of the right ventricle and left ventricle. The disease results in greater enlargement of the left atrium than of the left ventricle and is accompanied by a significant increase in left atrial "distensibility." Right and left heart pressures may be normal or may be increased; they tend to be elevated in the group with regurgitant fractions of over 50%. Annuloplasty results in marked clinical and hemodynamic improvement and may even be corrective.
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PMID:Hemodynamics and annuloplasty in isolated mitral regurgitation in children. 12 22

Left ventricular and myocardial performance were analyzed in 9 patients with chronic volume overload by mitral regurgitation from biplane cineventriculograms, simultaneous pressure recordings and cardiac output (thermodilution method) determinations. In spite of a considerable regurgitant fraction (49 +/- 17% of total stroke volume) cardiac index on the average is normal (CI = 3.3 +/- 0.7 l . min-1). The main compensatory mechanism to maintain cardiac ouput in hypertorphy (WED = 1.1 +/- 0.2 cm; LVMI = 216 +/- 62 g . m-2; LVMI/EDVI = 1.3 +/- 0.3 g . ml-1) and dilatation (EDVI = 163 +/- 37 ml . m-2). An increase of preload is of minor importance (PLVED = 15 +/- 7 mmHg; sigma ED = (40 +/- 19) x 10(3) dyn . cm-2). Left ventricular enlargement and wall mass are related to the degree of clinical heart failure (NYHA). Enddiastolic volume on the average is more increased than total stroke volume (89 +/- 31 ml . m-2). Ejection fraction (EF = 54 +/- 7%) was depressed despite a normal afterload (sigma tej = (171 +/- 37 x 10(3) dyn. cm-2; sigma max = (247 +/- 48 x 10(3) dyn . cm-2). The reduced ejection fraction and diminished myocardial power are related to an impairment of myocardial function (VMW . sigma tej = (83 +/- 39) x 10(3) dyn . cm-2 . s-1; VMW . sigma tej/ln sigma ED = 7.9 +/- 3.6 x 10(3) dyn . cm-2 . s-1). In comparable degrees of heart failure myocardial function is more compromised in patients with mitral than with aortic regurgitation.
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PMID:[Ventricular and myocardial function in mitral regurgitation (author's transl)]. 15 44

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.
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PMID:Evaluation of left ventricular performance in aortic stenosis, aortic regurgitation and mitral regurgitation from the stroke work/left ventricular mass ratio. 15 81

Cardiac catheterization, angiocardiography and ventricular muscle biopsy were performed in forty patients with idiopathic cardiomyopathy and included 21 cases of hypertrophic cardiomyopathy and 19 cases of congestive cardiomyopathy. 1) Cardiac catheterization revealed normal cardiac index and stroke index in both types, although there was a slight tendency toward decrease in cases of CCM. HCM showed slightly elevated right ventricular end-diastolic pressure and left ventricular end-diastolic pressure with a high incidence of atrial kick. CCM showed an elevated mean pulmonary artery, mean pulmonary wedge and left ventricular end-diastolic pressure. 2) Angiocardiographic findings revealed that in HCM left ventricular end-diastolic volume as well as left ventricular end-systolic volume, ejection fraction, meanVcf and MNSER were within normal range, and left ventricular anterior wall thickness, left ventricular mass and shortening of short axis in systole were increased. In CCM left ventricular end-diastolic volume and end-systolic volume increased, and ejection fraction, meanVcf, MNSER were decreased. The left ventricular anterior wall thickness was normal, and the left ventricular mass was smaller compared to the volume. The shortening of long and short axes in systole was slight. Left ventricular asynergy and mitral regurgitation occurred frequently. Coronary cineangiograms revealed normal patterns in both types. 3) Histological findings revealed hypertrophy of myofibers, degenerative changes, i.e. scarcity of myofibrils, deformity of nucleus and vacuolization of myocardial fibers, and collagen proliferation in both types. 4) No definite relationship was seen between parameters of left ventricular function and the findings of biopsied left ventricular muscle except for increase in wall thickness which might be apparently due to hypertrophy of the myocardial fibers.
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PMID:Angiocardiograms and hemodynamics in idiopathic cardiomyopathy, with reference to histology of biopsied ventricular myocardium. 15 67

Acute mitral regurgitation was produced in six open chest dogs by excising a portion of the anterior valve leaflet. Electromagnetic flow probes were placed in the left atrium around the mitral anulus and in the ascending aorta to determine phasic left ventricular filling volume, regurgitant volume and stroke volume. The systolic pressure gradient was calculated from simultaneously measured high fidelity left atrial and left ventricular pressures. The effective mitral regurgitant orifice area was calculated from Gorlin's hydraulic equation. Infusion of nitroprusside resulted in a significant reduction in mitral regurgitation. No significant change occurred in the systolic pressure gradient between the left ventricle and the left atrium because both peak left ventricular pressure and left atrial pressure were reduced. The reduction of mitral regurgitation was largely due to reduction in the size of the mitral regurgitant orifice. Reduction of ventricular volume rather than the traditional concept of reduction of impedance of left ventricular ejection may explain the effects of vasodilators in reducing mitral regurgitation.
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PMID:Mechanism of reduction of mitral regurgitation with vasodilator therapy. 42 14

Nineteen patients with mitral valve disease were studied before and a mean 11 months +/- 9 months following valve replacement or reconstruction, which resulted in good postoperative valve function. Biplane left ventricular angiography and pressures were utilized to determine end-diastolic volume/M. (EDV), end-systolic volume/M. (ESV), ejection fraction (EF), left ventricular mass/M. (LVM), and stroke work/M. (SW). There were 19 patients--six with mitral stenosis (MS), six with mitral stenosis and regurgitation (MS + MR), and seven with mitral regurgitation (MR). Those with MS and MS + MR preoperatively had no significant change in left ventricular end-diastolic pressure (LVEDP), EDV, ESV, LVM, or EF following surgery. Patients with MR had a significant reduction in LVEDP, EDV, SV, and SW. More importantly, the EF fell in four of these seven patients and LVM did not decrease following surgery. It is concluded that surgical treatment for MS and MS + MR had little effect on left ventricular performance. Following surgical treatment for MR, reduction in EDV is not associated with reduction in LVM, and frequently left ventricular performance deteriorates as judged by the EF.
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PMID:Left ventricular function before and following surgical treatment of mitral valve disease. 43 34

Nifedipine induces vascular smooth muscle relaxation through a calcium antagonistic action. The possibility of clinical use of the drug as a ventricular unloading agent has been explored in this study. In patients with hypertensive (seven cases), primary (seven cases) or rheumatic (aortic insufficiency five cases, mitral regurgitation five cases) cardiac disease, nifedipine, administered in a single sublingual dose (10 mg), relieved acute pulmonary edema. Circulatory variations from control were the following: decrease of systemic and pulmonary arterial pressures, and of vascular resistances, of pulmonary wedge pressure, of left ventricular diastolic and systolic dimensions (echocardiography); increase of cardiac and stroke index, of left ventricular mean rate of circumferential fiber shortening, of left and right mean pre-ejection delta P/delta t and mean rate of ejection; improvement of forward output in primary and rheumatic disease. Nifedipine benefits acute congestive heart failure by sustained fall of both preload and afterload and, possibly, by an enhanced contractility. It seems to have an appropriate indication in cases in which left ventricular afterload reduction is desirable.
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PMID:Clinical use of a calcium antagonistic agent (nifedipine) in acute pulmonary edema. 44 58

The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.
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PMID:Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area. 44 20

To compare the hemodynamic effect of vasodilator therapy on different regurgitant lesions, we infused sodium nitroprusside intraooperatively in 12 patients with mitral regurgitation and 15 with aortic regurgitation. During the critical period preceding establishment of cardiopulmonary bypass, both groups had developed intense vasoconstriction and cardiac decompensation. All demonstrated improved cardiac function with vasodilator therapy; however, the degree of improvement with nitroprusside differed in the two groups. Stroke volume increased 10 ml. per beat per meter squared in those patients with aortic regurgitation and only 6 ml. per beat per meter squared in those with mitral regurgitation (p less than 0.05). The percent increase in stoke volume induced by nitroprusside was inversely correlated to the preoperative left ventricular ejection fraction (r = 0.44, p less than 0.02). Patients with aortic regurgitation had lower preoperative left ventricular ejection fractions than those with mitral regurgitation (0.53 versus 0.63, p less than 0.02). Therefore, we conclude that patients with aortic regurgitation derived greater intraoperative hemodynamic benefit from unloading with nitroprusside, because they came to surgery with greater impairment of left ventricular contractility. Although nitroprusside improved cardiac function in both groups, only the patients with aortic regurgitation achieved normal pulmonary artery pressure (17 torr) and pulmonary vascular resistance (2.1 units) as a result of unloading. Those with mitral regurgitation continued to have pulmonary hypertension (28 torr) and increased pulmonary vascular resistance (3.9 units) despite vasodilator therapy. Thus the data suggest that patients with mitral regurgitation derived less hemodynamic benefit from intraoperative nitroprusside therapy because they were also limited by right ventricular dysfunction and a less responsive pulmonary vasculature.
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PMID:Comparison of intraoperative nitroprusside unloading in mitral and aortic regurgitation. 44 73


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