Valvular heart disease, Part 2. Mitral valve disease in older adults

Mitral valve disease is a common cause of morbidity and mortality in patients over age 65. The etiology, physical findings, and natural history of rheumatic mitral stenosis, rheumatic mitral regurgitation, chronic non-rheumatic mitral regurgitation, and acute mitral regurgitation may differ in older and younger patients. In addition, symptoms of mitral valve disease may be masked or exacerbated by coexistent coronary artery disease, pulmonary disease, hypertension, and other systemic disorders that commonly occur in older adults. The clinical evaluation, along with various non-invasive cardiac procedures, is important for identifying mitral valve disease as the cause of abnormal signs and symptoms in older patients. Recognition of mitral valve abnormalities has important implications, because mitral valve repair or replacement is usually associated with favorable short- and long-term results, even in patients over age 65.     

Results of coronary bypass and valve operations for mitral valve regurgitation

Combined coronary bypass grafting and valve procedures for mitral valve regurgitation result in poor outcomes, but the impact of the etiology of valve regurgitation on operative and long-term outcomes is not well defined. A retrospective analysis of 468 patients who had combined coronary bypass grafting and valve operations for mitral regurgitation showed that 78% had valve repairs and 22% had replacements for ischemic (45%) or degenerative (55%) disease. Predictors of operative mortality were ischemic mitral regurgitation, failure to use the internal mammary artery for grafting, severe coronary disease, acute myocardial infarction, low ejection fraction, advanced heart failure, emergency operation, and mitral valve replacement. The 5-year survival rates for propensity-matched patients with ischemic or degenerative disease were similar (66%). Low ejection fraction (< 35%), advanced age (> 67 years), valve replacement surgery, residual mitral regurgitation, and severe coronary artery disease were predictors of poor long-term outcome. Although the operative outcomes of ischemic mitral regurgitation were poor compared to those of degenerative disease, the long-term survival was similar in both groups of propensity-matched patients. Left ventricular remodeling, an optimal valve procedure without residual mitral regurgitation, and left ventricular function are more important determinants of long-term outcome than the etiology of valve regurgitation.     

Should a Regurgitant Mitral Valve Be Replaced Simultaneously with a Stenotic Aortic Valve?

Mitral valve regurgitation frequently accompanies aortic valve stenosis. It has been suggested that mitral regurgitation improves after aortic valve replacement alone and that the mitral valve need not be replaced simultaneously Furthermore, mitral regurgitation associated with coronary artery disease, particularly in patients with poor left ventricular function, shows immediate improvement after coronary artery bypass grafting. We studied 60 consecutive patients with aortic stenosis and mitral regurgitation to determine the degree of improvement in mitral regurgitation after aortic valve replacement alone versus aortic valve replacement combined with coronary artery bypass grafting. Thirty-six of the patients had normal coronary arteries (Group 1); the other 24 had symptomatic coronary artery disease requiring bypass surgery (Group 2). Echocardiography was performed preoperatively, 1 week postoperatively, and at follow-up. In Group 1, left ventricular ejection fraction did not improve early or at 2.5 months postoperatively, but mitral regurgitation improved gradually during follow-up. In Group 2, mitral regurgitation showed improvement 1 week postoperatively (p < 0.001), and left ventricular ejection fraction was improved at 2.5 months. We conclude that patients with aortic valve stenosis and mild-to-severe mitral regurgitation, without echocardiographic signs of chordal or papillary muscle rupture and without coronary artery disease, should undergo aortic valve replacement alone. The mitral regurgitation will remain the same or improve. For patients with coexisting coronary artery disease, simultaneous aortic valve replacement and coronary artery bypass grafting are imperative; however, the mitral valve again requires no intervention, since mitral regurgitation improves significantly after the other 2 procedures.     

Left atrial size,pressure, and v wave height in patients with isolated,severe, pure mitral regurgitation

In recent years, some concepts regarding the etiology and hemodynamics present in the syndrome of mitral regurgitation have changed. Coronary artery disease and mitral valve prolapse have replaced rheumatic heart disease as the most frequent cause of mitral regurgitation. Hemodynamic studies have shown that tall V waves in the pulmonary capillary wedge tracings are neither specific nor sensitive in detecting the presence of mitral regurgitation. In this study, we evaluated the role of various clinical, echocardiographic, and hemodynamic findings with regard to left atrial (LA) size, pressure, and V wave height. We found that the mean pulmonary capillary wedge pressure (PCW) and V wave height for the subset of patients with acute mitral regurgitation (PCW = 24.1 ± 10.9; V = 41.2 ± 20.7 mm Hg) was similar to the subset with chronic mitral regurgitation (PCW = 17.9 ± 7.5; V = 32.0 ± 18.2 mm Hg). In addition, we found that there was a significant logarithmic relationship between the LA size and the duration of the mitral regurgitation (y = 1.404 [log X] + 3.948; R = 0.678; p < 0.0005). Lastly, we found that LA size, compliance, regurgitant volume, and regurgitant valve orifice area all increase with time.     

Mitralinsuffizienz

Mitral regurgitation is the second most frequent reason for valve surgery. The most important causes of mitral regurgitation are degenerative valve disease (mitral valve prolapse), left ventricular impairment and dilatation (in coronary artery disease or dilated cardiomyopathy), and infective endocarditis. The regurgitation of blood from the left ventricle into the left atrium leads to dilatation of the left atrium, increase in pulmonary capillary pressure and pulmonary congestion. In chronic severe mitral regurgitation, the left ventricle dilates and becomes impaired over time. Key symptoms are fatigue and dyspnea on exertion. The most prominent physical sign is the characteristic systolic murmur. Echocardiography identifies severity, delineates morphology, and estimates the impact of mitral regurgitation on left ventricular function. Importantly, echocardiography identifies candidates for mitral valve repair. Symptomatic patients and asymptomatic patients with impaired left ventricular function should be operated. If possible, valve repair is preferred over valve replacement to better preserve left ventricular function and to avoid the need for postoperative anticoagulation (except if atrial fibrillation persists).     

Mitral regurgitation

Mitral regurgitation is the second most frequent reason for valve surgery. The most important causes of mitral regurgitation are degenerative valve disease (mitral valve prolapse), left ventricular impairment and dilatation (in coronary artery disease or dilated cardiomyopathy), and infective endocarditis. The regurgitation of blood from the left ventricle into the left atrium leads to dilatation of the left atrium, increase in pulmonary capillary pressure and pulmonary congestion. In chronic severe mitral regurgitation, the left ventricle dilates and becomes impaired over time. Key symptoms are fatigue and dyspnea on exertion. The most prominent physical sign is the characteristic systolic murmur. Echocardiography identifies severity, delineates morphology, and estimates the impact of mitral regurgitation on left ventricular function. Importantly, echocardiography identifies candidates for mitral valve repair. Symptomatic patients and asymptomatic patients with impaired left ventricular function should be operated. If possible, valve repair is preferred over valve replacement to better preserve left ventricular function and to avoid the need for postoperative anticoagulation (except if atrial fibrillation persists).     

A tale of two pressures: a case of pseudo-prosthetic mitral valve stenosis

We present a case of an 83-year-old female with past medical history of rheumatic fever associated mitral stenosis for which she underwent mitral commissurotomy 25 years prior to presentation. Subsequently, she underwent coronary artery bypass grafting and mitral valve replacement with a bio-prosthetic valve 8 years prior to presentation. Presently, she started experiencing worsening dyspnea and heart failure symptoms. Echocardiography showed mildly reduced left ventricular ejection fraction with severe aortic stenosis and pulmonary hypertension. The bioprosthetic mitral valve was functioning normally. We performed right and left heart catheterization for evaluation. Peak aortic gradient was 50 mm Hg with a mean gradient of 39 mm Hg. Aortic valve area was calculated to be 0.31 cm(2). However, simultaneous measurement of left ventricular and wedge pressures showed a significant gradient of 11 mm Hg across the mitral valve with a calculated mitral valve area of 0.4 cm(2). Because of discordant information between echocardiographic and hemodynamic data, we proceeded with trans-septal puncture to directly measure left atrial pressures. Simultaneous left atrial and left ventricular pressure measurement demonstrated a mean gradient of 4 mm Hg across the mitral valve with an area calculated at 1.9 cm(2). We review the tracings in detail and discuss the pitfalls of using pulmonary capillary wedge pressure as a surrogate for left atrial pressure.     

Frequency of acute myocardial infarction in valve repairs versus valve replacement for pure mitral regurgitation

Three hundred thirty-five consecutive isolated mitral valve operations for mitral regurgitation in patients with no significant coronary artery disease were reviewed over a 26-month period for the presence of a perioperative acute myocardial infarction (AMI). Of 224 patients undergoing mitral valve repair 12 (5.4%) had electrocardiographic and cardiac enzyme evidence of perioperative AMI develop. Of 111 patients undergoing mitral valve replacement none had perioperative AMI develop as determined by electrocardiographic and enzyme criteria (p = 0.01). All 12 infarctions after valve repair involved the inferior wall by electrocardiographic or echocardiographic criteria. Although no patient had significant clinical difficulty in recovery, 7 of the 12 patients (58%) were left with Q waves upon hospital discharge. The etiology of the AMI is believed to be air emboli introduced at the time of testing valve competence during left ventricular insufflation under pressure. Changes in surgical technique may reduce or eliminate this complication.     

M mode and cross-sectional echocardiographic recognition of fibrosis and calcification of the mitral valve chordae and left ventricular papillary muscles

The echocardiographic appearance of fibrotic thickening and calcification of mitral valve chordae tendineae and left ventricular papillary muscles in 17 patients is described. Pathologic proof of excessive fibrosis or calcification was obtained in five patients. In a sixth patient, calcium was demonstrated on angiography to extend from the chordae into papillary muscle. The characteristic feature of chordal and papillary muscle fibrosis and calcification is the presence of highly echogenic densities best visualized within the left ventricle at a level below the mitral valve leaflets. The more inferior location of these densities, within the body of the left ventricle, enables them to be easily differentiated from densities indicating fibrosis and calcification of the mitral valve anulus.The pattern of chordal and papillary muscle fibrosis and calcification was frequently associated with mitral anular calcification, aortic valve fibrosis or calcification and left atrial enlargement. One patient had rheumatic mitral valve disease. Many patients had mitral regurgitation and most had a history, physical examination and radiologie findings compatible with congestive heart failure. Although the origin and importance of the chordal and papillary muscle changes reported are not known, their frequent association with mitral regurgitation and with congestive heart failure suggests possible interrelations.     

Etiology and pathogenesis of thromboembolism.

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.     

Diastolic mitral regurgitation in acute but not chronic aortic regurgitation: implications regarding the mechanism of mitral closure

In acute aortic regurgitation, left ventricular pressure rises rapidly during diastole, which produces presystolic mitral valve closure. This does not occur in chronic aortic regurgitation. Since normal, nonregurgitant mitral valve closure may depend on properly coordinated atrial and ventricular contractions, we hypothesized that abnormal mitral valve closure occurring before systole in acute aortic regurgitation may produce diastolic mitral regurgitation detectable by Doppler echocardiography. Accordingly, we performed ultrasonic Doppler examination of seven patients with acute aortic regurgitation and 12 patients with chronic aortic regurgitation. Regurgitant aortic flow was severe in all cases. Doppler sampling within the left atrium demonstrated regurgitant mitral flow in late diastole in all patients with acute aortic regurgitation. The onset of diastolic mitral regurgitation coincided with mitral valve preclosure in patients with acute aortic regurgitation and occurred regardless of the position of the mitral leaflets at the initiation of closure. In contrast, none of the 12 patients with chronic aortic regurgitation had mitral valve preclosure or diastolic mitral regurgitation (p less than 0.05 versus acute aortic regurgitation). We conclude that diastolic mitral regurgitation accompanies mitral valve preclosure, which occurs in acute but not chronic aortic regurgitation. Thus diastolic mitral regurgitation may be a Doppler sign of acute aortic regurgitation, in the absence of a markedly prolonged PR interval. Furthermore, this observation suggests that normal, nonregurgitant mitral closure requires more than an increase in left ventricular pressure above left atrial pressure, regardless of the position of the mitral leaflets before closure.     

Mitral valve prolapse in patients with prior rheumatic fever

It is known that rheumatic heart disease frequently results in isolated mitral regurgitation without concomitant mitral stenosis, especially in countries with a high prevalence of rheumatic fever. However, more recent surgical pathologic data also have demonstrated a high incidence of mitral valve prolapse in cases of rheumatic heart disease, which suggests that rheumatic fever may be a cause of mitral valve prolapse. To determine whether this association of mitral valve prolapse and rheumatic heart disease is present in a stable clinic population, we studied 30 patients who had an apical systolic murmur and a well-documented history of rheumatic fever with dynamic auscultation, two-dimensional echocardiography, and pulsed Doppler examinations. Twenty of the 30 patients (67%) had findings on physical examination consistent with isolated mitral regurgitation and 25 patients (84%) had mitral regurgitation by Doppler examination. Echocardiography demonstrated mitral valve prolapse in 24 patients (80%), whereas only one of the total study group had echocardiographic findings consistent with mitral stenosis. We conclude that (1) the presence of an isolated systolic murmur in patients with a history of rheumatic fever frequently represents pure mitral regurgitation secondary to mitral valve prolapse and (2) postinflammatory changes in valvular tissue resulting from rheumatic fever may be the etiology of mitral valve prolapse in these patients.     

Doppler echocardiographic evaluation of ring mitral valvuloplasty for pure mitral regurgitation

Doppler echocardiographic studies were performed in 21 consecutive patients (mean age 56 +/- 11 years) to evaluate postoperative results of mitral ring anuloplasty. All patients were symptomatic and all had clinically severe isolated mitral regurgitation (MR). The origin of MR was myxomatous degeneration, coronary artery disease, rheumatic heart disease or congestive cardiomyopathy. In 20 patients ring anuloplasty was performed using the Carpentier ring and 1 patient using the Duran ring. Postoperative Doppler echocardiographic studies were performed to detect and semiquantitate residual MR by flow mapping and to identify left ventricular inflow or outflow obstruction. The severity of MR was assessed by flow mapping in the left atrium and graded from I to IV in increasing severity. Blood flow velocity spectra were recorded from the left ventricular outflow tract during systole and from the left ventricle subjacent to the mitral valve during diastole. Pressure half-time, mitral valve area and mitral valve gradient were derived from digitized mitral diastolic flow velocity spectra. After ring valvuloplasty, 9 patients had no MR and 6 had grade I, 3 grade II, 2 grade III and 1 patient grade IV MR. Peak diastolic mitral valve gradient was 8 +/- 4 mm Hg, mean diastolic gradient was 3 +/- 2 mm Hg and pressure half-time was 83 +/- 17 ms, representing a calculated mean mitral valve area of 2.9 +/- 0.8 cm. Peak velocity in the left ventricular outflow tract was 0.9 +/- 0.2 m/s, indicating no obstruction to outflow. Our study confirms that mitral ring valvuloplasty produces a significant reduction in severity of MR, and this is achieved without obstructing left ventricular inflow or outflow.     

Values for Mitral Valve Annulus Dimensions in Normals and Patients with Mitral Regurgitation

Objectives. The present study was designed to investigate the dimensions of mitral valve annulus in the presence of mitral regurgitation. Method. Fifty-four patients were examined. On transthoracic echocardiographic images, we performed linear measurements in the parasternal plane in order to define the size of the left ventricle, left atrium, and mitral valve annulus. We compared these findings with those obtained in 16 control subjects. Results. Twenty-one patients with mild or moderate mitral regurgitation demonstrated no significant change of the mitral valve annulus compared with the control group (P > 0.05). Seventeen patients with severe mitral regurgitation (grade of 4) had a significant increase of the dimensions of the mitral valve annulus, left ventricle, and left atrium (P < 0.05). The etiology of mitral regurgitation was degenerative in 32 patients, rheumatic in 2 patients, and mitral valve prolapse in 4 patients. All patients had normal left ventricular systolic function. Thirty-one patients were in normal sinus rhythm, and seven were in atrial fibrillation. Conclusions. The measurement of the diameter of the mitral valve annulus is feasible with transthoracic echo-cardiography. In addition to the evaluation of mitral valve leaflets and subvalvular apparatus, the measurement of the mitral valve annulus is important in the evaluation of mitral regurgitation, as its enlargement is indicative for severe mitral regurgitation .     

The clinical spectrum of tricuspid regurgitation detected by pulsed Doppler echocardiography

The clinical diagnosis of tricuspid regurgitation (TR) is often difficult. Two-dimensional pulsed Doppler echocardiography offers a sensitive and specific method for detecting and semi-quantitating tricuspid regurgitation. The clinical, radiographic, radionuclide, echocardiographic, and when available, the right cardiac catheterization findings were evaluated in 36 patients with a diagnosis of tricuspid regurgitation by pulsed Doppler. Ten healthy subjects served as controls. The underlying cardiac cause was rheumatic heart disease in 7 (20%), ischemic heart disease in 12 (33%), dilated cardiomyopathy in 5 (14%), hypertensive heart disease in 2 (5%), aortic valve stenosis and/or regurgitation in 3 (8%), mitral valve prolapse with mitral regurgitation in 1 (3%), and congenital heart disease in 6 (17%). Seven patients (19%) had a temporary or permanent transvenous right ventricular pacing wire. A systolic murmur was heard in 29 patients (81%) with 16 (46%) having an elevated jugular venous pressure. Tricuspid regurgitation was clinically suspected in only 2 patients (6%). Isolated tricuspid regurgitation was uncommon, seen in 6 patients (17%), and usually secondary to congenital heart disease, ischemic heart disease, with the use of a transvenous pacing wire and following mitral valve replacement. Right cardiac catheterization was performed in 10 patients, of which 7 demonstrated elevated right atrial and pulmonary artery pressure. Pulsed Doppler echocardiography offers a practical and accurate method of detecting and evaluating the severity of tricuspid regurgitation. Tricuspid regurgitation is generally a functional disorder, and frequently occurs in association with left sided valvular heart disease, cardiomyopathy or congenital heart disease.     

Plasma NT-proBNP is a potential marker of disease severity and correlates with symptoms in patients with chronic rheumatic valve disease

BACKGROUND: A noninvasive marker of disease severity and presence of symptoms is required in patients with chronic rheumatic valve disease (RVD). AIMS: We sought to test the utility of measuring of N-terminal pro-B type natriuretic peptide (NT-proBNP) in chronic phase RVD. We also evaluated whether echocardiographic measures are interrelated with NT-proBNP levels. METHODS: The study comprised 92 patients with RVD (mean age of 40+/-14 years) and 50 age/gender-matched control subjects. Functional status was assessed. Detailed echocardiographic examination was performed and mitral valve score was estimated. Venous blood samples were taken for measuring the level of NT-proBNP. RESULTS: The plasma levels of NT-proBNP rose with increasing severity of mitral valve stenosis (p<0.001), increasing severity of mitral valve score (p<0.001), increasing severity of clinical symptom (p<0.001), increasing severity of mitral regurgitation (p<0.013), presence of mitral valve calcification (p<0.001), presence of tricuspid valve stenosis (p<0.001), increasing severity of tricuspid regurgitation (p<0.011), presence of aortic stenosis (p=0.043), decreasing left ventricular ejection fraction (p<0.001), presence of left atrial thrombus (p=0.0019), and with increasing left atrium dimensions (p=0.002). CONCLUSION: NT-proBNP levels in patients with chronic RVD are a potential marker of disease severity and correlates with symptoms.     

Mitral valve prolapse in short-term experimental coronary occlusion: a possible mechanism of ischemic mitral regurgitation

Experimental coronary occlusions were carried out in 12 closed-chest dogs to investigate the functional anatomic characteristics of the mitral valve complex during acute myocardial ischemia. Two-dimensional echocardiography was used to assess left ventricular function, the mitral valve complex, and left atrial size. Presence of mitral regurgitation was assessed by left ventricular contrast echocardiography. Thirty-seven coronary occlusions of up to 10 min in duration were carried out in proximal or distal locations in the left anterior descending and the left circumflex coronary arteries. Mitral regurgitation, which was mild in severity as judged by a small rise in pulmonary artery wedge pressures, was observed in 15 of 37 brief coronary occlusion experiments. Mitral valve prolapse was noted in all 15 experiments, as well as in four additional studies in which mitral regurgitation was not seen. The development of experimental mitral valve prolapse was explained by measurements that demonstrated a relative displacement of the papillary muscle tips toward the mitral orifice. We conclude that mitral valve prolapse is a common sequela of short-term coronary occlusion and is often associated with mild mitral regurgitation. Relative displacement of ischemic papillary muscles toward the mitral orifice appears to be a likely mechanism of acute ischemic mitral valve prolapse.     

Differentiating clinical and echocardiographic characteristics of chordal rupture detected in patients with rheumatic mitral valve disease and floppy mitral valve: impact of the infective endocarditis on chordal rupture.

AIMS: We aimed to compare the clinical and echocardiographic correlates of chordal rupture in patients with rheumatic mitral valve disease and floppy mitral valve. METHODS AND RESULTS: The study group comprised of 224 patients who underwent transthoracic and transesophageal echocardiography because of the severe mitral regurgitation. Chordal rupture was detected in 58 (25.9%) out of the 224 patients, in 33 out of the 83 (39.7%) patients with floppy mitral valve, and in 25 out of the 141 (17.7%) patients with rheumatic mitral valve disease. Chordal rupture was more frequently associated with anterior leaflet (80%) in patients with rheumatic mitral valve disease, and posterior leaflet (72.7%) in patients with floppy mitral valve (p<0.05). Univariate correlates of chordal rupture were age, male sex, posterior mitral leaflet thickening and chordal elongation in patients with floppy mitral valve (p<0.05), and chordal shortening (p<0.0001) and infective endocarditis involving mitral anterior leaflet (p<0.05) in rheumatic group. Independent predictors of chordal rupture were age (>50 years), posterior mitral leaflet thickness (> or =0.45cm), and male sex (p<0.05) in patients with floppy mitral valve while infective endocarditis involving mitral anterior leaflet (p<0.05) in patients with rheumatic mitral valve disease. Patients with chordal rupture due to floppy mitral valve had an older age (p<0.0001), a male dominance, longer mitral leaflets and chordae, and a larger mitral annulus circumference (p<0.05) as compared to those with rheumatic chordal rupture. Despite the comparable severity of mitral regurgitation and left atrial diameters between the two groups of chordal rupture (p>0.05), functional class and pulmonary artery systolic pressure were higher, and atrial fibrillation, acute deterioration, infective endocarditis, mitral leaflet rupture and need for mitral valve surgery in the 3 months were more frequent in rheumatic chordal rupture subgroup (p<0.05). CONCLUSION: Chordal rupture seems to be more frequently associated with anterior mitral leaflet in rheumatic mitral valve disease, whereas it was the posterior leaflet in floppy mitral valve. Chordal rupture was related to male sex, older age, posterior leaflet thickening, and chordal elongation in patients with floppy mitral valve. However, infective endocarditis, acute deterioration, and need for early mitral surgery were more frequent in patients with rheumatic chordal rupture.     

Mitral valve prolapse due to coronary artery disease

Controversy exists concerning the etiologic role of coronary artery disease in the prolapsing mitral valve leaflet syndrome. A 35 year old man with progressive coronary artery disease is described. Auscultation before and after his first myocardial infarction revealed only a fourth heart sound; subsequent left ventricular cineangiography demonstrated normal anatomy and function of the mitral valve, despite extensive wall motion abnormalities. Six months later he experienced another myocardial infarction after which the typical mid-systolic click, late systolic murmur of mitral valve prolapse developed. A second left ventricular cineanglogram at this time revealed mid-systolic mitral valve prolapse and mitral regurgitation. This patient's course indicates that myocardial damage from coronary artery disease can cause mitral valve prolapse in patients without preexisting redundant mitral valve tissue.     

风湿性心脏病合并非冠状动脉粥样硬化性心肌梗死的临床及冠脉造影分析

目的探讨慢性风湿性心脏病（风心病）合并心肌梗死的原因、临床特征、冠状动脉造影表现及治疗.方法回顾性分析18例风心病合并心肌梗死患者的临床和冠脉造影资料.结果18例患者中二尖瓣病变15例（83.3%）,其中5例合并主动脉瓣病变;单纯主动脉瓣病变3例;11（61.1%）例已行瓣膜置换术,服用华法令治疗,国际标准比值（INR）维持在2.0～2.5.合并心房颤动15例（83.3%）.18例患者均有突发胸痛病史,心电图显示前壁心肌梗死13例（72.2%）,下壁心肌梗死5例（27.8%）,其中Q波心梗7例（38.9%）,非Q波心梗11例（61.1%）.伴有心肌酶增高.冠状动脉造影显示冠脉正常14例（77.8%）,4例为急性栓塞,其中1例发生于常规冠脉造影中,另3例胸痛时造影分别为对角支、前降支及右冠脉堵塞,经介入治疗再通.全部患者存活.结论并发于风心病的心肌梗死很少见,冠状动脉栓塞是引起心肌梗死的原因,梗死部位多为前壁,延迟冠脉造影多数正常.