Cardiology. acute severe mitral regurgitation

Acute mitral regurgitation occurs as a complication of myocardial infarction in perhaps 1% of cases. The characteristic clinical findings include a new systolic murmur occurring in the setting of sudden development of acute congestive heart failure, hypotension, and shock. S3 and S4 gallops and sinus rhythm usually are present, and gross left ventricular or left atrial enlargement usually is not evident radiologically. The immediate and long-term prognoses for patients with acute severe mitral regurgitation are poor without treatment. Although medical therapy can reverse temporarily some of the hemodynamic aberrations, it does not influence survival or eliminate the need for surgical treatment. Surgery consisting of mitral valve replacement and possibly simultaneous coronary revascularization appears to offer some hope in increasing the survival rate among these patients. When acute severe mitral regurgitation is secondary to rupture of chordae tendineae in circumstances other than coronary artery disease, the outlook is not as grim. These patients may show signs and symptoms of congestive heart failure for a few weeks or, at times, many months. Again, sinus rhythm usually is present, with slight left ventircular enlargement, a relatively normal left atrial size, and markedly elevated left atrial and pulmonary arterial pressures. This constellation of findings is indicative of a large mitral regurgitant flow with preservation of left ventricular function and suggests that the patient is likely to benefit greatly from surgical treatment. The prognosis for such patients is much better than it is for the patients with acute mitral regurgitation secondary to coronary artery disease.     

Combined surgery for mitral regurgitation associated with extensive annular calcification and left main coronary artery disease

Although extensive calcification of the mitral annulus is encountered infrequently, it presents a formidable problem in mitral valve surgery. We describe a case of severely calcified mitral annulus associated with grade IV mitral regurgitation in addition to left main coronary artery disease. The patient was a 66-year-old woman who successfully underwent thorough excision of the calcified bar, annular reconstruction with a autologous pericardial strip, mitral valve replacement with a mechanical prosthesis, and double coronary artery bypass grafting using arterial grafts.     

Mitral annulus size in isolated mitral stenosis

M-mode and two-dimensional echocardiographic images were obtained using the planimeter method in the short axis view and calculated by Doppler-derived pressure half-time in 24 patients with mitral stenosis before and after surgical commissurotomy and posterior annuloplasty. The diameter of the mitral valve annulus was measured in the standard long axis view and in the apical four-chamber view using two-dimensional echocardiography. Preoperatively, the mitral annulus was dilated in all patients as a consequence of left atrial dilation. This could be one of the factors causing residual regurgitation after surgical mitral commissurotomy. However, more data are needed to demonstrate that annuloplasty can prevent the development of mitral regurgitation after surgery.     

Comparison of the Carpentier and Duran prosthetic rings used in mitral reconstruction

This clinical study was undertaken to evaluate the Duran flexible ring and the Carpentier rigid ring in terms of mitral annulus motion, transmitral flow and left ventricular function. Twenty-six patients (11 receiving rigid rings and 15, flexible rings) with normal sinus rhythm and with no or only trivial mitral valve regurgitation after surgical repair were selected. Angiograms demonstrated no significant differences in left ventricular systolic function between the two groups of patients. The area of the mitral annulus with the flexible ring significantly changed during the cardiac cycle. There were significant differences in the left ventricular fractional shortening (rigid ring, 35.8%; flexible ring, 43.4%) and in the peak velocity (rigid ring, 222 cm/s; flexible ring, 186 cm/s) at peak exercise. These data suggest that the flexible ring interferes less with the normal movements of the mitral annulus during the cardiac cycle, and that, under exercise conditions, it performs better than the rigid ring. We therefore conclude that mitral valve reconstruction using the Duran flexible ring is advantageous in patients with mitral regurgitation due to degenerative disease and sinus rhythm.     

The cumulative risks of prolapsing mitral valve. 40 years of follow-up

Prolapsing mitral valve is a common cardiac condition, occurring in approximately 16 million people in the United States alone. Primary prolapsing mitral valve may be familial or nonfamilial and may be associated with myxomatous degeneration of the mitral valve leaflets, such as occurs in Marfan syndrome and other connective tissue disorders. Secondary forms may be associated with such entities as rheumatic fever (especially after commissurotomy) and coronary artery disease (in the presence of ruptured chordae tendineae), and with such congenital conditions as interatrial defect and primary cardiomyopathy with outflow tract obstruction. Prolapsing mitral valve is characterized by late systolic murmur, mid-systolic click, or both. Arrhythmias occur in the form of benign premature atrial contraction, premature nodal contraction, and paroxysmal atrial tachycardia. As the patient ages, atrial flutter and atrial fibrillation tend to develop. In some chronic cases, especially those involving atrial fibrillation, systemic emboli may occur. Rare premature ventricular contractions may be largely benign, whereas more frequent premature ventricular contractions may lead to severe arrhythmic complexes such as ventricular tachycardia or ventricular fibrillation. With advancing age, atrioventricular conduction defects of varying degrees or sick sinus syndrome may necessitate a pacemaker installation. About one quarter of prolapsing mitral valve cases progress, with increasing mitral insufficiency and increasing enlargement of the left atrium and left ventricle, which at times leads to congestive heart failure. Coronary artery disease may occur with the severity commensurate with the patient's age group. About three quarters of patients with prolapsing mitral valve syndrome lead normal lives.     

Aortic homograft and mitral valve repair in a patient with Werner's syndrome

We report the case of a 66-year-old man suffering from Werner's syndrome (adult progeria); he presented with several cardiac disorders, including coronary artery disease, aortic stenosis, and mitral regurgitation, mainly due to calcific deposits in the mitral annulus and the aortic cusps. Treatment consisted of mitral repair, homograft replacement of the aortic valve, and coronary artery bypass grafting. Avoidance of prosthetic material because of chronic infectious skin ulcers constituted the main goal of the operation.     

Reoperation for valvular heart diseases

To elucidate the limitation of mitral valve reconstruction, 53 mitral disease patients (Mitral stenosis: 29, Mitral regurgitation: 24) undergoing reoperation late after valve reconstruction were studied, taking account of valvular lesions at initial operation. Reoperation rate after open mitral commissurotomy for mitral stenosis was higher in the patients with valvular regurgitation at initial operation than in those with severe subvalvular lesions or calcified valve. Reoperation rate for mitral regurgitation after mitral valvuloplasty was higher in the patients with stenotic fibrous degeneration or dilated annulus at initial operation than in those with torn chorda. Thus, these findings suggest that combined lesion of stenosis and regurgitation at initial operation may affect the reoperation rate in patients undergoing mitral valve reconstruction for either mitral stenosis or mitral regurgitation. Different approaches to the mitral valve through the left atrium and various techniques of the atriotomy have been practiced according to the need for a particular patients. The left atrium and the mitral valve can be exposed through median sternotomy followed by biatrial atriotomy or transplant approach. A correct approach and good exposure plays a key role in the success of redo surgical procedure for mitral valve disease.     

Diagnostic localization of insulinoma. Experiences with 25 patients with solitary tumors

A 71-year old man presented with partial rupture progressing to complete rupture of the left ventricular anterior papillary muscle after acute anterolateral myocardial infarction. The progressive rupture was demonstrated by transthoracic and transesophageal echocardiography. Transthoracic echocardiography showed exaggerated systolic prolapse of the anterior mitral leaflet with grade III mitral regurgitation and partial disruption of the anterolateral papillary muscle, but transesophageal echocardiography during surgery disclosed the progression of the partial rupture to complete rupture. The flail anterior mitral leaflet with severe mitral regurgitation and the head of the ruptured papillary muscle into the left atrium in systole were confirmed. The patient was treated by coronary artery bypass grafting and mitral valve prosthesis using a St. Jude Medical valve with good outcome.     

Non-obstructive hypertrophic cardiomyopathy with mitral regurgitation requiring valve replacement

Non-obstructive hypertrophic cardiomyopathy (HCM) is rarely associated with mitral regurgitation severe enough to require valve replacement. A 39-year-old man, previously diagnosed as having non-obstructive HCM with mitral regurgitation, developed atrial fibrillation with tachycardia and congestive heart failure. Echocardiography and cardiac catheterization, including left ventriculography, documented an unusual type of non-obstructive HCM with severe mitral regurgitation. The patient underwent successful mitral valve replacement.     

A case report of infective endocarditis with total rupture of the posterior papillary muscle after aortic valve replacement

We reported a case with severe mitral regurgitation caused by total rupture of the posterior papillary muscle two days after aortic valve replacement. A 62-year-old man was transferred to our hospital with high fever and dyspnea with severe aortic regurgitation caused by infective endocarditis. The left heart failure occurred suddenly two days after the initial operation. Echocardiogram revealed massive mitral regurgitation and rupture of the posterior papillary muscle. He underwent emergent mitral valve replacement. Histological examination of the papillary muscle showed typical ischemic necrosis without inflammation. The postoperative course was uneventful. We suggested the papillary muscle rupture in this case may be due to coronary artery emboli occurred in association with infective endocarditis.     

Atrial macroreentry involving the myocardium of the coronary sinus: a unique mechanism for atypical flutter

Atrial flutter involving either clockwise or counterclockwise rotation around the tricuspid annulus utilizing the subeustachian isthmus has been well described. However, macroreentrant atrial circuits in atypical atrial flutter in patients who have not undergone previous surgery or without atrial disease are not well defined. We describe a patient without structural heart disease who presented with an atrial macroreentrant rhythm. Entrainment mapping demonstrated a critical isthmus within the coronary sinus. Activation mapping demonstrated double potential throughout the length of the coronary sinus with disparate activation sequences. A circuit involving the myocardium of the coronary sinus, exiting in the lateral left atrium, down the interatrial septum, and reentering into the coronary sinus was identified. Successful ablation of the rhythm was accomplished by a circumferential radiofrequency application within the coronary sinus.     

A rare case of 2 free thrombi in left atrium with mitral stenosis

A 64-year-old female was admitted with general fatigue and orthopnea. Preoperative echocardiography showed a free ball thrombus in the left atrium, mitral stenosis and severe tricuspid regurgitation. To avoid a herniation of thrombus to the mitral orifice, an emergency operation was performed. Two free and small mural thrombi were found in the left atrium. Thrombectomy, mitral valve replacement and tricuspid annuloplasty were performed successfully. Postoperative course was uneventful, and she was discharged in good condition on the 21st postoperative day.     

Myxoma of the mitral valve prolapsing into the left atrium and ventricle: report of a case

A rare case of myxoma originating from the mitral valve is reported. A 25-year-old woman was found to have a mobile mass around the mitral valve that prolapsed into the left atrium and the left ventricular outflow tract. The mitral valve was approached via the left atrium and aorta, and was excised completely along with the tumor; it was thus replaced with a mechanical prosthesis. The patient recovered and demonstrated no signs of recurrence 16 months postoperatively.     

Left atrial isolation for chronic atrial fibrillation caused by mitral valvular stenosis and regurgitation

Surgical isolation of the left atrium was performed for the treatment of chronic atrial fibrillation secondary to mitral valvular disease in a 65-year-old woman who underwent mitral valvular replacement. Left atrial isolation was simple procedure, prolonging the usual paraseptal atriotomy toward the both mitral valvular commissures anteriorly and posteriorly. The incision was conducted two centimeters apart from the mitral valve annulus, and cryoablation was added at the edges to ensure isolation of the residual left atrium. We suggest performing this simple procedure in patients with chronic atrial fibrillation undergoing mitral valvular replacement, in whom correction of irregular beat and compromised hemodynamics can be obtained.     

Damage to the circumflex coronary artery during mitral valve repair with sliding leaflet technique

We report a case of damage to the circumflex coronary artery during mitral valve repair using sliding leaflet technique in a patient with a posterior mitral leaflet prolapse and coronary artery disease who underwent mitral valve reconstruction using Carpentier's technique and coronary artery bypass grafting. This case underscores the risk of circumflex coronary artery injury during mitral valve reconstruction, especially in patients with left coronary dominance or codominance, and therefore emphasizes the importance of knowing the coronary artery anatomy preoperatively. The use of intraoperative transesophageal echocardiography is mandatory for the evaluation of mitral valvuloplasty.     

Structural basis for changes in left ventricular function and geometry because of chronic mitral regurgitation and after correction of volume overload

Left ventricular function and myocyte structure were examined in three groups of dogs: (1) 3 months of mitral regurgitation caused by chordal rupture (n = 7); (2) chronic mitral regurgitation followed by mitral valve replacement and a 3-month recovery period (n = 7), and (3) sham controls (n = 8). The left ventricular end-systolic stiffness constant (Kess) was measured as an index of left ventricular contractile function with stress-strain relationships obtained by cinecatheterization. Isolated myocyte structure and composition were examined with computer-assisted morphometry and nuclear area computed with deoxyribonucleic acid fluorescence. Left ventricular contractile function was significantly depressed with chronic mitral regurgitation compared with control values (Kess, 2.1 +/- 0.1 versus 3.6 +/- 0.2; p < 0.05) and returned to control values with mitral valve replacement (3.8 +/- 0.2). Left ventricular mass significantly increased in both the mitral regurgitation and mitral valve replacement groups compared with control values (121 +/- 10, 120 +/- 5 versus 95 +/- 9 gm, respectively; p < 0.05). Myocyte length increased with mitral regurgitation beyond control values (194 +/- 4 versus 218 +/- 8 microns; p < 0.05) and increased beyond mitral regurgitation values after mitral valve replacement (231 +/- 7 microns; p < 0.05). Myocyte volume with mitral regurgitation increased slightly beyond control values (33.5 +/- 0.7 versus 37.6 +/- 1.3 microns3; p = 0.15) and significantly increased with mitral valve replacement (40.1 +/- 1.2 microns3; p < 0.05). Myocyte myofibril volume significantly declined with mitral regurgitation compared with control values (14.8 +/- 1.5 versus 22.2 +/- 0.7 microns3; p < 0.05) and significantly increased beyond both mitral regurgitation and control values with mitral valve replacement (27.1 +/- 1.1 microns3; p < 0.05). Myocyte nuclear area with mitral regurgitation remained unchanged from control values (1430 +/- 122 versus 1163 +/- 89 microns2) but increased significantly with mitral valve replacement (2209 +/- 250 microns2; p < 0.05). In summary, the left ventricular contractile dysfunction with chronic mitral regurgitation is accompanied by increased myocyte length and reduced myofibril content. In contrast, the left ventricular hypertrophy and improved left ventricular pump function with mitral valve replacement were due to increased myocyte volume and increased contractile protein content.     

Ventricular buckling: a factor in the abnormal ventriculogram and peculiar hemodynamics associated with mitral valve prolapse

Because of intractable ventricualr arrhythmias after a near-fatal episode of ventricular fibrillation, a patient with idiopathic mitral valve prolapse was subjected to mitral valve replacement. Vector analysis and intraoperative epicardial mapping localized the ectopic focus to the region of the posterior papillary muscle. The patient is alive and well two years after surgery; chronically inverted T waves have become upright. But propranolol and diphenylhydantoin are needed to prevent arrhythmias and T wave abnormalities during standing and exercise. Preoperatively, with the onset of mitral regurgitation and a second rapid phase of prolapse, the ventriculogram was deformed by abnormal midsystolic hyperkinesis at both sites of papillary muscle insertion. Postoperatively, focal hypokinesis appeared in the same areas, implying that they had been retracted by the prolapsing valve. Preoperatively, a papillary tip could be seen entering the mitral ring while coronary arteriography showed late systolic elongation of a small vessel feeding the anterior papillary muscle, suggesting that the papillary apparatus was indeed subject to damaging stress during the abnormal basal movement. Three other persons with severe mitral prolapse (but intact chordae) have had valve repacement and developed qualitatively similar changes in the ventriculogram. Papillary speciments in two showed significant fibrosis. Indication for operation in one of these was edpisodic ventricular fibrillation, which has not recurred. A spectrum of ventriculographic abnormality associated with mitral prolapse could be partly explained by hypokinesis of the papillary loops, variably disguised by retraction stress tansmitted from the billowing leaflets, translocation of blood into the expanding valve sail, and various degrees of unloading into the left atrium. Abnormal intraventicular flow may probably result from associated prolapse of the anterior leaflet and from buckling of the papillary sties toward the mitral annulus. Unusual physical findings in the operated cases and in eight other patients define a clinically recognizable syndrome in which severe prolapse abbreviates left ventricular ejection. Liability to symptoms and to progression of disease seems high in this group.     

Surgical treatment of ventricular septal defect and ruptured sinus of Valsalva associated with infective endocarditis

Two patients with ventricular septal defect of Kirklin type I and ruptured right coronary sinus of Valsalva associated with infective endocarditis were operated on. Both had bacillus vegetation clinging to the aortic and pulmonary valves and the right ventricular intimal wall around the septal defect. Aortic and pulmonary regurgitation were also found. The surgical approach included vertical incision of the right ventricular outflow tract and pulmonary trunk and transverse aortotomy. The right coronary sinus of Valsalva showed distinct aneurysmal change in one patient. The aortic valve and infected Valsalva sinus were excised in both cases, and the pulmonary valve and right ventricular wall where infection extended thoroughly débrided. The resulting defect, including the ventricular septal defect and excised right Valsalva sinus and aortic annulus, was closed with one patch, and the prosthetic valve inserted in the position of the original aortic valve using this patch as part of the annulus. Both patients had a good postoperative course and are doing well, although slight pulmonary regurgitation persists.     

Artificial chordae in the treatment of anterior mitral leaflet pathology

This report describes the authors' clinical experience with expanded polytetrafluorethylene (e-PTFE) sutures to replace the anterior mitral leaflet chordae for valve repair. Between November 1986 and July 1995, 203 patients underwent operations with e-PTFE chordae insertion. Among these, 122 had artificial chordae utilized for anterior mitral leaflet repair. Four patients had the valve replaced during the same operation because of an unsatisfactory result. One patient died from respiratory insufficiency 16 days after operation. Transoesophageal echocardiography at discharge from hospital showed no evidence of regurgitation in 81 cases, and trivial regurgitation in 36. During a mean follow-up of 36.6 (range 1-106) months two other patients died from causes unrelated to the valve repair, while one patient had a transient ischaemic attack returning to sinus rhythm. Two patients were reoperated on 12 and 18 months respectively after their initial operation for progression of valvular degeneration causing natural chordae rupture. Among the remaining 113 patients, 111 are in New York Heart Association functional class I and yearly transoesophageal echocardiography has shown absent or trivial regurgitation. The utilization of e-PTFE as artificial chordae for anterior mitral leaflet pathology is a safe and reliable procedure, yielding excellent results and increasing the number of candidates for valve repair.     

Relation between mitral orifice surface area and extent of hemodynamic disorder of the pulmonary circulation in patients with mitral stenosis

Mitral annulus and valves form the mitral orifice area with the size between 4.0-6.0 cm2. Every area which is smaller than this, represents mitral stenosis. As a consequence of mitral stenosis hemodynamic gradients occur over the mitral orifice with circulation disturbances below and above the stenotic mitral valve. The size of transmitral gradient is important in the evaluation of functional or/and structural changes in the blood vessels of pulmonary circulation. This investigation included 40 patients with mitral stenosis (or accompanying minimal mitral regurgitation). All patients underwent echocardiographic examination: area of the mitral orifice was determined and hemodynamic procedure with the left and right heart catheterization was performed. The following hemodynamic parameters were measured: mean capillary wedge pressure, left ventricular filling pressure, left ventricular mean diastolic pressure, mean pulmonary artery pressure. According to these parameters resistance in the pulmonary circulation was measured. The size of the mitral orifice was determined according to oximetry blood analyses and hemodynamic parameters. All patients were divided into 4 groups: minimal (2.5-4.0 cm2), mild (1.5-2.5 cm2), moderate (1.0-1.5 cm2) and severe mitral stenosis (1.0 cm2). The comparison of echocardiographic and hemodynamic parameters revealed a high and positive correlation between the area of mitral orifice. There was also a negative and moderate correlation between the values of stenotic mitral orifice area and total pulmonary resistance, i.e. in all patients with severe mitral stenosis there was an increased pulmonary arteriolar resistance. CONCLUSION: Noninvasive echocardiographic method is valid in the evaluation of stenotic mitral valve area. In the evaluation of hemodynamic parameters in the pulmonary circulation the index of arteriolar pulmonary systemic vascular resistance is very important. In all patients with the area of stenotic mitral orifice 1.0 cm2, there are functional or pathomorphologic changes in the pulmonary circulation of the blood vessel wall.