Special Article - Exercise-induced right ventricular injury or arrhythmogenic cardiomyopathy (ACM): The bright side and the dark side of the moon.

There is still debate on the range of normal physiologic changes of the right ventricle or ventricular (RV) function in athletes. Genetic links to arrhythmogenic cardiomyopathy (ACM) are well-established. There is no current consensus on the importance of extensive exercise and exercise-induced injury to the RV. During the intensive exercise of endurance sports, the cardiac structures adapt to athletic load over time. Some athletes develop RV cardiomyopathy possibly caused by genetic predisposition, whilst others develop arrhythmias from the RV. Endurance sports lead to increased volume and pressure load in both ventricles and increased myocardial mass. The extent of volume increase and changes in myocardial structure contribute to impairment of RV function and pose a challenge in cardiovascular sports medicine. Genetic predisposition to ACM may play an important role in the risk of sudden cardiac death of athletes. In this review, we discuss and evaluate existing results and opinions. Intensive training in competitive dynamic/power and endurance sports leads to specific RV adaptation, but physiological adaptation without genetic predisposition does not necessarily lead to severe complications in endurance sports. Discriminating between physiological adaptation and pathological form of ACM or RV impairment provoked by reinforced exercise presents a challenge to clinical sports cardiologists.

Use of a pigtail catheter to engage a difficult internal mammary artery.

Increasing use of bilateral internal mammary arteries for coronary surgery will increase the number of interventions in these grafts. Such interventions may be technically challenging because of often tortuous and angulated vessels. We describe a technique to intubate an acutely angulated right internal mammary artery that was inaccessible with conventional catheters.

C/T polymorphism of the intercellular adhesion molecule-1 gene (exon 6, codon 469). A risk factor for coronary heart disease and myocardial infarction.

BACKGROUND: The intercellular adhesion molecule-1 (ICAM-1) mediates the interaction of activated endothelial cells with leukocytes and plays a fundamental role in the pathogenesis of coronary atherosclerosis. ICAM-1 single-base C/T polymorphism, which determines an amino acid substitution in the ICAM-1 protein in exon 6 codon 469, has been described. Our purpose was to determine whether this C/T polymorphism influences the risk of coronary heart disease (CHD) and myocardial infarction (MI) in humans. METHODS AND RESULTS: We enrolled 349 patients with angiographically documented CHD, including a sub-group of 179 patients with acute or chronic MI. The control group consisted of 213 patients with normal left ventricular function and no documented evidence of CHD. All patients and controls were Germans genotyped by polymerase chain reaction and allele-specific oligonucleotide techniques for the ICAM-1 polymorphism. In the patients with CHD and MI the frequencies of the T genotype (TT+TC) were significantly higher than the CC genotype compared to the control subjects (P<0.001). With the additional use of multivariable logistic regression analysis for CHD (TT+TC versus CC; P=0.011, odds ratio 2.21, 95% CI 1.20-4.07), we found a significant association between CHD and MI and the TT and TC genotype of the ICAM-1 gene polymorphism. CONCLUSIONS: These results suggest that the TT and TC genotype of the ICAM-1 gene polymorphism in codon 469 is a genetic factor that may determine an individual's susceptibility for CHD and MI.