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At least 19 recordsLinked to original sources
PubMed1979

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

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.

Adult↗
PubMed1979

Indications for surgical replacement of the mitral valve. With particular reference to common and uncommon causes of mitral regurgitation.

Mitral valve replacement is considered when there is severe mitral stenosis, severe mitral insufficiency or a combination of the two. Ordinarily, surgical replacement is considered only for patients who are in functional classes III or IV and do not respond to medical management. Patients with symptomatic mitral stenosis should be treated with mitral commissurotomy whenever possible. Patients selected for commissurotomy should have a pliable valve, no other major valve dysfunction, sinus rhythm, no systemic embolism and good left ventricular function. Early operation is not ordinarily required. Mitral insufficiency may require mitral valve replacement in six rather common settings: rheumatic disease, rupture of mitral chordae tendineae, postinfarction rupture of a papillary muscle, intractable infective endocarditis, floppy mitral valve and malfunction of a prosthetic valve. Rupture of mitral chordae tendineae can usually be recognized from the history, physical examination, echocardiogram and angiocardiogram. Severe left ventricular papillary muscle dysfunction is usually due to cardiac infarction, and occurs within the first 9 days of infarction. When only a papillary muscle tip is ruptured the patient may survive long enough for a mitral valve replacement. In infective endocarditis, operation is more often needed because of congestive heart failure than because of refractory infection. Evidence of mitral stenosis or insufficiency in a patient with a previously implanted prosthetic valve usually indicates an urgent need for study and early operation. Uncommon causes of mitral incompetence that may require valve replacement are endocardial fibroelastosis, Marfan's syndrome, calcified mitral anulus, osteogenesis imperfecta, methysergide-induced heart disease and carcinoid heart disease.

Adult↗
PubMed1977

Mitral regurgitation in coronary heart disease.

Mitral reguritation is a relatively common finding in coronary heart disease. In this series of 127 patients, selected with a view to coronary or left ventricular surgery on the basis of severity of symptoms, the incidence was 39 (31%). Mitral regurgitation is significantly more common in patients with a history or electrocardiographic evidence of previous myocardial infarction. Clinically it may present as a pan- or late systolic or even a mid-systolic, ejection type murmur at the apex or at the left sternal edge; but in 39 per cent of the patients with angiographic mitral regurgitation no murmur was present. Angiographically important mitral regurgitation (grades 2-4/4) was usually associated with a systolic murmur; this finding was independent of ejection fractions. Left ventricular enlargement clinically or radiographically is likely to accompany mitral regurgitation but left atrial enlargement (electrocardiographically or on chest x-ray) is a more reliable pointer to mitral regurgitation and pulmonary venous hypertension is even more strongly suggestive of its presence. The electrocardiographic signs of papillary muscle infarction were rare in this series (15%) and were not related to angiographic mitral regurgitation. There was no difference in the incidence of mitral regurgitation in association with anterior or inferior myocardial infarction or in distribution of coronary artery disease. There is, however, a higher incidence of mitral regurgitation in more severe coronary arterial disease (P less than 0-05). The incidence of mitral regurgitation is significantly higher with reduction in left ventricular ejection fraction (P less than 0-001), with rise in the left ventricular end-diastolic pressure (P less than 0-02), and with abnormal contraction patterns, but the severity of mitral regurgitation is not significantly related to these findings.

Adult↗
PubMed1978

Beneficial effects of hydralazine in severe mitral regurgitation.

The severity of mitral regurgitation is, in part, determined by aortic impedance to left ventricular outflow. Sodium nitroprusside acutely decreases regurgitant flow, but the importance of its dual vasodilating effects, the lowering of peripheral vascular resistance and increasing of venous capacitance, is unclear. We studied the hemodynamic response to intravenous hydralazine, which selectively acts on the arteriolar resistance bed, in 10 patients with severe mitral regurgitation. Hydralazine produced a 50% increase in forward stroke volume (22 +/- 2 to 33 +/- 3 ml/m2, P less than 0.001) and a 33% reduction in regurgitant stroke volume (40 +/- 6 to 27 +/- 6 ml/m2, P less than 0.001), with a resultant fall in pulmonary capillary wedge v wave and mean pressures. Unlike nitroprusside, it did not alter left ventricular end-diastolic volume or pressure. Oral hydralazine maintained this hemodynamic improvement for at least 48 hours and, in three patients, provided more sustained clinical improvement. We conclude that hydralazine, by virtue of its selective lowering of aortic impedance, reduces the amount of mitral regurgitation and thus may be a useful mode of interim or chronic therapy in selected patients.

Adult↗
PubMed1979

Mechanism of reduction of mitral regurgitation with vasodilator therapy.

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.

Animals↗
PubMed1977

The effects of left ventricular load and contractility on mitral regurgitant orifice size and flow in the dog.

Acute mitral regurgitation (MR) was produced in 12 dogs by closed chest partial valvulectomy and the relative contributions of MR pressure gradient (MRG), the time for regurgitant flow (VSI), and the MR orifice area (MRA) to mitral regurgitant volume (MRV) assessed. Aortic and left atrial pressures, biplane left ventricular (LV) angiography, forward flow and mitral regurgitant flow (MRF) were measured following MR induction and following augmentation of left ventricular end-diastolic volume (EDV), increased aortic resistance (angiotensin), and in the presence of increased ventricular contractility (calcium or epinephrine). Mitral regurgitation orifice area was determined by calculation and the diameters of the mitral anulus and subvalvular areas measured angiographically. Angiotensin and volume infusion induced a substantial increase in MRF which was largely dependent on an increase in MRA but not MRG, while augmentation of contractility decreased MRF accompanied by a decrease in MRA, relatively independent of MRG. Left ventricular size and shape are major determinants of MRA and resultant MRF in acute mitral regurgitation. These findings may help to explain the effects of such factors as ventricular loading and volume on the clinical course of mitral regurgitation in man.

Animals↗
PubMed1979

Dynamic changes in the canine mitral regurgitant orifice area during ventricular ejection.

We designed this study to test the hypothesis that in acute mitral regurgitation the mitral regurgitant area (MRA) is a dynamic quantity which varies with the time variation of ventricular volume. Mitral insufficiency was created in five open-chest dogs in which a portion of the anterior leaflet was excised. Phasic aortic and mitral flows were measured electromagnetically, along with left atrial and ventricular pressures. Filling, regurgitant, and stroke volumes, and systolic pressure gradient were determined by digital methods. MRA was calculated from the fluid dynamic equation of motion to give the temporal mean and the instantaneous value at three instants of time and at the time of peak flow (when inertia is negligible). Mean regurgitant fraction was 42 +/- 12% with no indication of left ventricular failure due to volume overload. MRA decreased monotonically with time to 59% of its initial value and closely paralleled the decrease in ventricular volume during systole. In a control study using a tilting-disc prosthesis with a hole 5 mm in diameter in the occluder, the calculated MRA was time invariant and equal to the measured area for regurgitation. We conclude that in acute mitral regurgitation the MRA is a function of ventricular volume.

Animals↗
PubMed1979

Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area.

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.

Angiotensin II↗
PubMed1979

Secundum atrial septal defect and significant mitral regurgitation: incidence, management and morphologic basis.

To better understand the association between mitral regurgitation and secundum atrial septal defect and to clarify the evaluation and management of these patients, the records of 235 adult patients with atrial septal defect were reviewed. Ten patients (4 percent) had significant mitral regurgitation defined by clinical, hemodynamic and angiographic criteria. Three patients required mitral valve replacement at the time of closure of the atrial septal defect and four patients had closure alone, one of whom required mitral valve replacement after five years. Three patients did not undergo closure of the atrial septal defect or mitral valve replacement because of severe coexisting medical problems. In six patients, the mitral valves were studied pathologically and all had thick, fibrotic leaflets and short, thick, fibrotic chordae tendineae. Three of these valves also had scattered areas of patchy myxomatous degeneration and three had areas of vascular ingrowth suggestive of rheumatic disease. Although both invasive and noninvasive studies have high-lighted the coincidence between atrial septal defect and mitral regurgitation, particularly the frequent association of mitral valve prolapse, our data indicate that this association rarely has clinical significance. Furthermore, the morphologic basis for mitral regurgitation in patients with atrial septal defect consists of leaflet and chordal thickening fibrosis and deformity rather than attenuation and ballooning as would be expected in mitral valve prolapse.

Adult↗
PubMed1975

Silent mitral regurgitation.

The occurrence of significant mitral regurgitation whithout the characteristic auscultatory signs, particularly the holosystolic murmur and the third heart sound, is unusual. It becomes of considerable importance when it occurs in combined lesions of the mitral valve, and more so in those areas where the treatment of mitral stenosis is by closed mitral valvotomy. Two cases of silent mitral incompetence are presented. The features that should have indicated the coexistence of regurgitation with mitral stenosis were cardiomegaly with considerable dilatation of the left atrium, and lesser degrees of right ventricular hypertrophy on electrocardiography for the severity of mitral stenosis and evidence of biventricular hypertrophy.

Adult↗
PubMed1976

Pure mitral regurgitation. Etiology, pathology and clinical patterns.

The varied etiology of pure mitral regurgitation is demonstrated in this clinicopathological study, comprising 59 surgically treated cases with this condition. One third of the cases was of rheumatic origin, one fifth had ischemic heart disease, another fifth floppy valves and one eighth an isolated rupture of the chordae with necrosis of the chord matrix. To our knowledge the histopathological findings in the last group have not been described before. Congenital mitral regurgitation, bacterial endocarditis and cardiomyopathy were rare causes of mitral regurgitation. Differences between the groups were observed in the sex ratio, duration of history, auscultatory findings ECG signs, compliance of the left ventricle and in the morphological findings.

Adult↗
PubMed1977

Ventriculographic and hemodynamic features of mitral regurgitation of cardiomyopathic, rheumatic and nonrheumatic etiology.

Quantitative angiographic findings were reviewed in 40 patients with significant mitral regurgitation classified into three etiologic groups: group I, primary mitral regurgitation (prolapse, ruptured chordae); group II, mixed stenosis and regurgitation of rheumatic origin; and group III, cardiomyopathic mitral regurgitation. For patients in both groups I and II, left ventricular end-diastolic volume was directly related to regurgitant fraction, and ejection fraction was generally well maintained. In contrast, patients in group III had a depressed ejection fraction (less than 0.40) and end-diastolic volume that was disproportionately increased in relation to the degree of regurgitation. Left ventricular end-diastolic pressure was a poor indicator of severity of regurgitation in all patient groups. There was a significant negative correlation between forward cardiac index and regurgitant fraction. There was significant relation, although with considerable variation, between the normalized V wave and regurgitant fraction. The graphs of chamber size, ejection fraction and hemodynamic measures plotted against the severity of regurgitation in different patient groups provide a perspective for interpreting the findings in individual patients.

Angiocardiography↗
PubMed1977

Echocardiographic diagnosis of mitral regurgitation in congestive cardiomyopathy.

Eighteen patients with congestive cardiomyopathy were studied by echocardiography and cardiac catheterization. Patients with coronary disease on angiography or primary valvular disease were excluded. Six patients showed mild or no mitral regurgitation; in 12 others the degree of mitral regurgitation was moderate or severe. The echocardiographic features in these patients were: (1) a dilated left ventricle (LV), (2) normal LV wall thickness, (3) reduced LV posterior wall motion, and (4) reduced or absent systolic thickening of the interventricular septum (IVS). IVS motion was reduced in 10 patients, and appeared "normal" or increased in another eight, all of whom showed moderate or severe mitral regurgitation on angiography. It is concluded that an apparent normal or increased motion of the IVS with reduced or absent systolic thickening in congestive cardiomyopathy is evidence for coexistence of significant mitral regurgitation. Reduced or absent systolic thickening can distinguish these patients from those with segmental myocardial disease and normal septa or dilated LV's due to volume overload.

Cardiomyopathies↗
PubMed1978

Intermittent severe mitral regurgitation.

The findings in two patients with hemodynamic evidence of intermittent severe mitral regurgitation with cyclic variation in right and left ventricular pressures are presented. Both patients had aortic and mitral valvular regurgitation of unknown etiology without definite evidence of papillary muscle dysfunction. The basis for the variation in the degree of mitral regurgitation is unclear.

Aortic Valve Insufficiency↗
PubMed1979

Dynamic geometry of the left atrium and left ventricle in acute mitral regurgitation.

The instantaneous transverse diameter of the left atrium, left ventricular free wall segment length (SEG), and the long axis of the anterior papillary muscle (APM) length were measured throughout the cardiac cycle, using ultrasonic dimension gauges together with left atrial and left ventricular pressures in 12 open-chest dogs. During atrial contraction, left atrial diameter decreased from 19.7 to 18.7 mm, while left ventricular dimensions increased simultaneously. During ventricular ejection, percent shortening was 26% in SEG and 10% in APM, while atrial diameter increased continuously to 20.5 mm, with a concomitant rise in the v wave of left atrial pressure. After normal mitral valve opening, left atrial diameter decreased rapidly simultaneously with the y descent of atrial pressure. Graded mitral regurgitation was then produced by sectioning the chordae tendineae. With moderate mitral regurgitation, end-diastolic length of the SEG increased by 27%, while extent of shortening (delta L) was augmented by 96%. End-diastolic length of the APM increased by 7%, and delta L was augmented by 60%. Left atrial pressure was sharply elevated, with a distinct a wave followed by the more prominent v wave. End-diastolic diameter of the left atrium was enlarged to 22.9 mm with increased atrial shortening and expansion. As mitral regurgitation was increased to a severe degree by additional chordal rupture, end-diastolic length and delta L continued to increase both in SEG and APM. Left atrial pressure was further elevated (a wave 25 mm Hg and v wave 47 mm Hg). Left atrial end-diastolic diameter further increased in 24.9 mm. However, the amplitude of left atrial shortening and expansion decreased remarkably. In severe mitral regurgitation, isoproterenol and nitroprusside decreased left atrial pressure and diameter, restoring more forceful atrial shortening.

Acute Disease↗
PubMed1976

Sudden interruption of leaflet opening by ventricular contractions: a mechanism of mitral regurgitation.

The motion of both mitral cusps and the presence of valvular regurgitation during ventricular contractions were investigated in seven experiments on dogs in which radiopaque markers had been sutured to the cusps and the valve annulus 1-32 wk before the studies. Cineangiograms of the left ventricle were obtained during ventricular ectopic beats, interposed throughout the cardiac cycle (20-99% of cycle length) and during induced variations in the P-R interval (0-200 ms). Mitral regurgitation was observed only during a) weak, early ectopic beats (peak pressure below 34 mmHg) which were incapable of closing the cusps and b) when ventricular contractions suddenly interrupted normal leaflet motion toward the ventricle, during three well-defined periods of diastole (diastolic valve opening, diastolic rebound, and atrial opening). Valve closure following sudden reversal of cusp opening was slow and the leaflets often did not arrive simultaneously at their closed positions. These findings suggest that sudden interruption of leaflet opening by ventricular contractions is an important mechanism of transient mitral regurgitation in the normal heart.

Animals↗
PubMed1976

Mitral regurgitation secondary to ruptured chordae tendineae: clinical, hemodynamic and electrocardiographic findings.

The clinical, hemodynamic, and electrocardiographic findings in 11 patients with mitral regurgitation secondary to ruptured chordae tendineae are presented. Left atrial overloading, as manifested by a large terminal negative force in the P wave of lead V1, was present in 8 of the 11 patients. Six of the eight patients with this atrial abnormality had a normal size or minimally enlarged left atrium on chest x-ray films and angiography. Left ventricular hypertrohpy was present in 7 of the 11 patients and appeared to be related to the duration of cardiac symptoms. It is concluded that a large terminal negative force in the P wave in lead V1 is a useful clinical indicator of increased left atrial pressure in mitral regurgitation of recent onset. The electrocardiographic finding of left atrial overloading is to be expected in most cases of mitral regurgitation secondary to rupture of the chordae tendineae.

Adult↗