Red wine consumption, coronary calcification, and long-term clinical evolution

Coronary artery calcification (CAC) is associated with atherosclerotic complications. However, elevated CAC may not always imply a worse prognosis. Herein, we report the clinical evolution of long-term red wine (RW) drinkers in relation to CAC. We followed 200 healthy male habitual RW drinkers and compared them to 154 abstainers for a period of 5.5 years. The initial evaluation included coronary computed tomography angiography (CTA), clinical, demographics, and laboratory data. CAC was quantified by the Agatston score. The follow-up process was conducted by telephone calls and/or hospital record review. The composite end-point of total death, acute myocardial infarction (AMI), or coronary revascularization (or major adverse cardiac event - MACE) was assessed. The RW drinkers ingested 28.9±15 g of alcohol/day for 23.4±12.3 years. They had higher high-density lipoprotein and low-density lipoprotein, but lower C-reactive protein than abstainers. Age, total cholesterol, triglycerides, glucose, and liver enzymes were similar. History of diabetes was lower among drinkers, but other risk factors were similar. However, drinkers had higher CAC than abstainers; the mean value was 131.5±362 in drinkers vs 40.5±320 in abstainers (P<0.001). The median and interquartile range were 15 (0.0-131.5) in RW drinkers and 1 (0.0-40.5) in abstainers (P=0.003). During the follow-up, MACE was significantly lower in drinkers than in abstainers, despite their higher CAC. The difference was driven mainly by AMI (0 vs 6; P<0.03). Greater CAC values in this setting did not predict worse prognosis. A possible underlying mechanism is lesion calcification, which leads to plaque stabilization and less clinical events.

Fistulas arteriovenosas pulmonares microscopicas. / Microscopic pulmonary arteriovenous fistula

Se comunica el caso de un varon de 15 anos de edad en quien se establecio el diagnostico de fistulas arteriovenosas pulmonares microscopicas. Su sintomatologia basica era disnea y cianosis progresivas de 3 y 2 anos respectivamente. El examen fisico, con excepcion del hipocratismo digital, era normal. La radiografia de torax y el electrocardiograma eran tambien normales. En las pruebas de funcion respiratoria se encontraba hipoxemia severa (PaO2 = 41 mmHg), cuyo mecanismo fisiopatologico fundamental era el de aumento importante del cortocircuito veno-arterial (Qs/Qt). La localizacion de este Qs/Qt, fue intensamente investigada a traves de fono y ecocardiografia y por cateterismo derecho, los que resultaron normales. La angiografia pulmonar no mostro alteraciones significativas. A pesar de ello, un estudio de ecocardiografia con contraste realizado en cavidades ventriculares sugirio la existencia del cortocircuito a nivel intrapulmonar, dato que fue ratificado por el estudio hemodinamico con oclusiones selectivas de las ramas de la arteria pulmonar realizado con cateter de Dotter-Lucas, el que demostro aumento del cortocircuito en ambos pulmones. El estudio histopatologico de la biopsia pulmonar confirmo el diagnostico de fistulas arteriovenosas microscopicas intrapulmonares