Predictors of systemic embolism in patients with mitral stenosis. A prospective study

BACKGROUND: Most studies of the predictors of systemic embolism in patients with mitral stenosis have been retrospective. OBJECTIVE: To prospectively study factors associated with systemic embolism in mitral stenosis. DESIGN: Prospective cohort study. SETTING: University-affiliated medical institution with 3000 beds. PATIENTS: 534 consecutive patients with a mitral valve area of 2.0 cm2 or less; 132 patients were in sinus rhythm, and 402 were in atrial fibrillation. MEASUREMENTS: Nine clinical and 10 echocardiographic variables were assessed for prediction of systemic embolism over a mean (+/- SD) follow-up of 36.9 +/- 22.5 months. Diagnosis of systemic embolism was based on symptoms and signs (sudden onset of peripheral arterial ischemic or neurologic manifestations without prodromes) and on findings on computed tomography, angiography, and surgery. RESULTS: For patients in sinus rhythm, age (relative risk [RR], 1.12 [95% CI, 1.04 to 1.21]), the presence of a left atrial thrombus (RR, 37.1 [CI, 2.82 to 487.8]), mitral valve area (RR, 16.9 [CI, 1.53 to 187.0]), and the presence of significant aortic regurgitation (RR, 22.4 [CI, 2.72 to 184.8]) were positively associated with embolism. For patients in atrial fibrillation, previous embolism (RR, 3.11 [CI, 1.66 to 5.85]) was positively associated with embolism; percutaneous balloon mitral commissurotomy (RR, 0.37 [CI, 0.18 to 0.79]) was a negative predictor. CONCLUSIONS: It may be prudent to give anticoagulants not only to patients in atrial fibrillation and patients with previous systemic embolism but also to those showing a left atrial thrombus or significant aortic regurgitation on echocardiography. Early percutaneous balloon mitral commissurotomy may also help prevent systemic embolism in patients with mitral stenosis.     

Relation of systemic arterial pulse pressure to coronary atherosclerosis in patients with mitral stenosis

The relation of a wide systemic arterial pulse pressure to coronary atherosclerosis has not been fully defined. One hundred fifty-nine patients > 40 years old with symptomatic mitral stenosis (MS) who received routine coronary angiography were classified into 2 groups according to the presence of > or = 50% diameter narrowing of > or = 1 coronary artery (n = 48) or no significant disease (n = 111). Pulse pressure was determined both by noninvasive sphygmomanometer and invasive catheterization methods. There were no significant differences in risk factors of coronary artery disease (CAD) or the severity of MS between the 2 groups. From multivariate logistic regression analysis, independent predictors of development of CAD in MS were age (standardized coefficient beta = 1.3437, p = 0.0025), gender (beta = 0.0107, p = 0.0105), mean blood pressure (beta = 1.1839, p = 0.0105), and pulse pressure (beta = 1.3157, p = 0.0008). A wide pulse pressure (> or = 60 mm Hg) correlated with the presence of angiographically significant CAD with a sensitivity and specificity of 88% and 77%. The negative predictive value was 93%. Pulse pressure assessed by sphygmomanometry provided important clinical information. A wide pulse pressure in patients with MS was associated with a high incidence of CAD.     

Calcific cerebral embolism in systemic calciphylaxis

Calciphylaxis represents a rare complication of end-stage renal disease with hyperparathyroidism. We report the case of a 26-year-old woman with systemic calciphylaxis secondary to chronic renal failure who developed mitral annular calcification and a right middle cerebral artery stroke. The high-density lesion seen on CT scan of the brain probably represents a calcified cerebral embolus originating from the mitral valve.     

Pathology of mitral valve stenosis and pure mitral regurgitation--Part I

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis are reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenital malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation will be discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendinae.     

Causes of recurrences of mitral stenosis

The authors present an analysis of the late results of closed mitral commissurotomy in 364 patients (maximum terms of observation--17 years). Main causes of recurrent mitral stenosis were recognized: activation of a rheumatic process (50%), nonspecific scarring processes (27%), inadequate commissurotomies (11.1%) and others (11.1%). The routine antirheumatic therapy (bicillin+salicylates) was found to be ineffective in prophylaxis against mitral restenoses. Recurrent mitral stenosis proved to occur more frequently in patients operated upon in young age (under 30).     

Propranolol in mitral stenosis during sinus rhythm

Patients with early symptomatic mitral stenosis usually suffer from pulmonary congestion on the basis of left atrial and pulmonary venous hypertension. They are often in sinus rhythm, and cardiac output is usually well maintained. Symptoms occur most often when heart rate, cardiac output, or both are increased. In this study, intravenous propranolol administered to patients with pure mitral stenosis in sinus rhythm resulted in significant reductions in mitral diastolic gradient (-7.1 mm. Hg +/- 1.6 SED), mean pulmonary wedge pressure (--6.9 mm. Hg +/- 1.2) and mean pulmonary artery pressures (--9.0 mm. Hg +/- 1.2). This was due to simultaneous reduction of heart rate (--13.0 beats/minute +/- 2.6 and cardiac output (--0.5 L./minute +/- 0.2). A small associated reduction of left ventricular systolic pressure (--5.1 mm. Hg +/- 2.6) was not accompanied by adverse clinical effects. A potential role for propranolol in medical management of pure mitral stenosis in the presence of sinus rhythm is suggested.     

Coronary atherosclerosis in subjects with mitral stenosis

The coronary arteries were examined in 60 specimens from patients with mitral stenosis. In three, localized obstruction was nonatherosclerotic in nature (in one, arterial dysplasia; in two, embolic). In 18 of the remaining 57 cases (31.5%), significantly obstructive atherosclerosis in one or more segments of the coronary arterial system was found. This represented 46% of the males and 27% of the females. The incidence of involvement of three or more arteries by significantly obstructive atherosclerosis was 39%, while in a cited series of subjects with angina pectoris three or more vessels were involved in 79% of the cases. It may be concluded that, on the average, the distribution of lesions in patients with mitral stenosis and significant coronary atherosclerosis is less wide than in subjects with clinical coronary disease.     

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.     

Diagnosis and differential therapy of mitral stenosis

The aim of this study was to investigate the role of metabolic activation in the olfactory toxicity of methyl iodide (MeI). Adult male rats were exposed via nose-only inhalation to 100 ppm MeI for 0-6 h, and non-protein sulphydryl (NP-SH) concentrations determined in selected tissues. Depletion of NP-SH occurred in all tissues, but was most marked and rapid in the respiratory epithelium of the nasal cavity and the kidney. Olfactory, lung and liver NP-SH levels were affected to a lesser extent, and those of the brain declined by only 20-30% over the whole time course. In order to modulate glutathione (GSH) status, animals were pre-treated with (1) phorone plus L-buthionine sulphoximine (BSO), which depleted NP-SH levels in all the tissues examined, or (2) the isopropyl ester of GSH (IP-GSH), which was shown to replenish NP-SH concentrations in all tissues except the liver of animals previously administered phorone. When animals were pre-treated with phorone plus BSO and then exposed to 100 ppm MeI for 2 h, there was a potentiation of the toxicity of MeI as judged by the clinical observations on the animals. In contrast, treatment with IP-GSH prior to and during exposure to MeI for 4 h afforded a marked protection to the olfactory epithelium. In order to inhibit cytochromes P450, animals were pre-treated with cobalt protoporphyrin IX. This decreased hepatic cytochrome P450 concentrations by > 90%, but when animals were then exposed to 100 ppm MeI for 4 h there was no effect on the severity of the olfactory lesion. These results indicate that conjugation of MeI with GSH is a detoxification rather than an activation pathway. Also, there is no major role for cytochrome P450-dependent oxidation in the development of the olfactory lesion.     

Early changes of respiratory function in mitral valve stenosis

In order to detect early changes of respiratory function in patients affects by pure mitral valve stenosis, the authors selected 12 patients-non smokers, without symptoms of respiratory disease, of I and II NYHA class. In all subjects right and left cardiac catheterization and conventional spirometric measurements were performed. Then maximal mid-expiratory flow (MMEF), maximal expiratory flow at 50% of vital capacity (MEF 50%), maximal expiratory flow at 25% of vital capacity (MEF 25%), closing volume (CV) and closing capacity (CC) were determined, to find a small airways (bronchi of caliber inferior to 2 mm) disease. Whereas conventional spirometric measurements showed normal values, the small airways disease was proved by MEF 50% and MEF 25% measurements. The small airways obstruction observed by the authors may be due to: a) dilatation of pulmonary vessels because of venous congestion resulting in the compression of adjacent small airways; b) partial bronchiolar obstruction because of congestion of submucous venous plexus; c) interstitial oedema due to increase of extravascular pulmonary water because of pulmonary venous congestion.     

Percutaneous mitral balloon valvotomy in a patient with coexistent mitral stenosis and hypertrophic cardiomyopathy

A patient with coexistent mitral stenosis and hypertrophic cardiomyopathy is described, in whom symptoms related to impaired left ventricular diastolic filling improved after successful percutaneous mitral balloon valvotomy.     

Bronchial hyperresponsiveness before and after percutaneous transluminal mitral commissurotomy in patients with mitral stenosis

To study the effects of percutaneous transluminal mitral commissurotomy (PTMC) on bronchial responsiveness to inhaled methacholine in patients with mitral valve stenosis (MS), methacholine inhalation tests and pulmonary function tests were done in 10 patients with MS before and one week after PTMC. The mean log cumulative dose producing a 35% decrease in respiratory conductance (PD35Grs) was significantly higher after PTMC in nine patients in whom PTMC was successful (p < 0.05). There were no significant changes in the results of pulmonary function tests after PTMC. One patient had severe mitral regurgitation after PTMC, and a decrease in PD35Grs. Six of the other nine patients in whom PTMC was successful continued to be hyperresponsive to inhaled methacholine. These data show that bronchial hyperresponsiveness in patients with MS is less severe after PTMC, concomitant with the relief of pulmonary congestion, and they suggest that the remaining bronchial hyperresponsiveness is responsible for peripheral airway narrowing with organic remodeling.