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We review the clinical files of patients who entered the Regional General Hospital No. 20 IMSS in the City of Tijuana Mexico between May 1994 and May 2004 with diagnosis of primary acute pericardial disease. Patients diagnosed as having active tuberculous pericardial effusion were eligible for the study. Twenty-one were included in the study (14 men and 7 women). The aged ranged from 16 to 48 years (mean 36 years). The diagnosis was made by the following studies: identification of tubercle bacilli in the pericardial fluid or tissue (n = 4), identification of caseating granulomas in the pericardium or elsewhere (n = 2), positive culture for Mycobacterium tuberculosis in pericardial fluid (n = 8), in pleural fluid (n = 1), sputum culture (n = 3), gastric aspirate samples (n = 1), lymph node biopsy (n = 1), and pericardial effusion without obvious cause, responding to antituberculous therapy (n = 5). The clinical, laboratory, electrocardiography, radiographic, and echocardiography features were analyzed. We review in each patient follow-up, pericardial fluid cytology, and pericardial biopsy, if available. All patients had pericardial effusion; nine (42.8%) patients had cardiac tamponade. Pericardiocentesis was performed in 16 patients, "therapeutic" pericardiocentesis was performed in 43.7%, and "diagnostic" pericardiocentesis was performed in 56.2% all cases. Constrictive pericarditis developed in two patients, all required partial pericardiectomy. All patients received triple antituberculous chemotherapy. No patient died.

A 33 year-old man developed coccidioidomycosis which resulted in pericarditis associated with congestive heart failure. A pericardial effusion developed and progressed to constrictive pericarditis. A pericardiectomy was performed and revealed that the pericarditis was due to Coccidioides immitis. The patient died after surgery. This is the second case of coccidioidomycosis with pericarditis reported in Mexico's literature.

In this report we describe the case of a 19-year-old woman who had right-sided hemiparesis. In search of a source of embolism, we performed transthoracic echocardiography, which showed a large, complex, and irregular multilobulated left ventricle mass adherent to the endocardial surface. Open-heart surgery was performed. The mass was removed, and histologic examination confirmed the thrombotic material with focal regions of calcification. The diagnosis of antiphospholipid antibodies syndrome was confirmed by an anticardiolipin antibodies test.

Infective endocarditis is a frequent complication in intravenous drugs abusers. It is evident that in recent years this problem has increases as a consequence of the growing number of drug addicts. We review the clinical files of patients who entered the Regional General Hospital No. 20 IMSS in the City of Tijuana Mexico between May 1994 and May 1998 with diagnosis of infective endocarditis and had evidence intravenous abuse. Eight patients were included in the study. None of them had preexisting valve abnormalities. The infection involved right-sided values in 62.5% of cases left-sided values in 12.5%, and both sides in 12.5% of cases Staphylococcus aureus was the infecting germ in 50% of the cases. Survival of patients with right infective endocarditis was 75% and only 25% of them required surgical intervention. The mortality of infection in left side was 75% and 100% if infection involved both sides. Infective endocarditis in drugs abusers has a favorable prognosis when right sided valves are affected. Mortality rates are higher in patients with left-sided involvement.

An asymptomatic 15-year-old woman was studied because of a systolic ejection murmur. The echocardiogram showed a mobile, leaflet-like structure attached to the ventricular surface of the anterior mitral leaflet, chordae tendineae and papillary muscle. This structure moved to the left ventricular outflow tract during systole occupying the subaortic area. Conventional Doppler examination revealed left ventricular outflow obstruction caused by the accessory mitral valve tissue that produced a pressure gradient of 25 mmHg between the aorta and left ventricle. The diagnosis was not obvious clinically and was based on the echocardiographic data.

In this study we evaluate prospectively a new color Doppler method for calculating the mitral valve area based on identifying a blue-red aliasing interfase proximal to the orifice, corresponding to the flow convergence region (FCR). This method can be used to calculate areas using the continuity equation. We studied 61 patients with stenosis. The mitral valve area was calculated using pressure half-time (PHT) Doppler method which were compared with values that obtained by the FCR method, according to the following formula. AVM (cm2) = 2 pi r2 x VN/Vmax; where "r" is the FCR radius measured from the orifice to the first color aliasing (blue-red interface); VN is Nyquist velocity and Vmax is the peak flow velocity by continuous wave Doppler. Twenty three patients had pure mitral stenosis and 38 double mitral lesion. Twenty patients were on sinus rhythm while 41 in atrial fibrillation. Calculated mitral valve area using the FCR method correlated well with mitral valve area determined by PHT method at a correlation coefficient of r = 0.96 (y = 0.097 x + 54.9, SEE = 0.10 cm2, p < 0.001). MVA by FCR ranged from 0.4 to 2.5 cm2 (mean = 1.19 cm2). MVA by PHT ranged from 0.42 to 2.48 cm2 (mean = 1.15 cm2). Color Doppler FCR method provides an accurate estimate of effective mitral valve area and may be useful as an alternative to the pressure half-time method. The calculated mitral valve area by the FCR method is not influenced by the presence of mitral regurgitation nor atrial fibrillation.