The prevalence of isolated right ventricular infarction is 0.4-2.4% in autopsy series and may occur by at least three different mechanisms, of which occlusion of a nondominant right coronary artery is reviewed here. Although rare, as oxygen demand/supply of the right is lower than that of the left ventricle, due to the smaller muscular mass, and it has a good prognosis, sudden death and cardiac rupture have been reported. Differential diagnosis with anterior infarction is needed. ECG may help but specific criteria should be adopted: dome-like and decreasing ST segment elevation from V1 to V3 leads; rapid ST segment normalization and no Q wave evolution from V1 to V3 leads, either accompanied or not by modest ST segment elevation in DIII (but not aVF) evolving in no Q wave; ST segment elevation in right-sided leads which should be explored; absence of ST segment depression in aVL; absent concomitant ST segment elevation in all inferior leads (DII, DIII, aVF). Applying these criteria may prevent erroneous management of right ventricular infarction if it is confused with left ventricular infarction. Right ventricular function evaluation should always be performed by echocardiography. Magnetic resonance imaging should be useful. An illustrative case and an ECG flow-chart are presented.

In this patient population the use of IABP, but not thrombocytopenia per se, is a possible primary cause of worse ischemic outcomes.

Epidemiologic differences in ischemic heart disease incidence between women and men remain largely unexplained. The reasons of women’s “protection” against coronary artery disease (CAD) are not still clear. However, there are subsets more likely to die of a first myocardial infarction. The purpose of this review is to underline different treatment strategies between genders and describe the role of classical and novel factors defined to evaluate CAD risk and mortality, aimed at assessing applicability and relevance for primary and secondary prevention. Women and men present different age-related risk patterns: it should be important to understand whether standard factors may index CAD risk, including mortality, in different ways and/or whether specific factors might be targeted gender-wise. Take home messages include: HDL-cholesterol levels, higher in pre-menopausal women than in men, are more strictly related to CAD. The same is true for high triglycerides and Lp(a). HDL-cholesterol levels are inversely related to incidence and mortality. In primary prevention the role of statins is not completely ascertained in women although in secondary prevention these agents are equally effective in both genders. Weight and glycemic control are effective to reduce cardiovascular disease (CVD) mortality in women from middle to older age. Blood pressure is strongly and directly related to CVD mortality, from middle to older age, particularly in diabetic and over weighted women. Kidney dysfunction, defined using UAE and eGFR predicts primary CVD incidence and risk in both genders. In secondary prediction, kidney dysfunction predicts sudden death in women in conjunction with left ventricular ejection fraction evaluation. Serum uric acid does not differentiate gender-related CVD incidences, although it increases with age. Age-related differences between genders have been related to loss of ovarian function traditionally and to lower iron stores more recently. QT interval, physiologically longer in women than men, may be an index of arrhythmic risk in patients with mitral valve prolapse and increased circulating levels of catecholamines. However, there are no large population-based studies to assess this. In conjunction with novel parameters, such as inflammatory markers and reproductive hormones, classical risk score in women may be implemented in the future.