A 62 year old man with severe angina pectoris underwent aoroto-coronary saphenous vein graft implantation. After a four month asymptomatic period the patient underwent aorto-coronary graft angiography. Left anterior descending graft opacification demonstrated multiple venous aneurysmal dilations. The clinical significance of this finding is currently unknown but such saphenous vein disease warrants further investigation. Saphenous vein grafts have been utilized to replace or bypass obstructed and diseased peripheral arteries such as those of the carotid and femoral-popliteal vascular systesm. In 1967 Favaloro introduced the saphenous vein as a means for bypassing local obstructions in diseased coronary arteries of human subjects. Since the advent of the aorto-coronary saphenous vein bypass graft procedure several studies have reported pathologic alterations of these grafts at post-mortem examination or at the time of re-operation. Other investigators have also noted changes in these venous grafts when they have been implanted in peripheral vessels. We report here a patient with aneruysmal dilations of an aorto-coronary artery saphenous vein bypass graft. Furthermore, possible mechanisms which might produce such venous aneurysms and the clinical significance of such an entity are discussed.

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Background: While certain P-Wave morphologies have been associated with abnormal atrial size and either pulmonary or cardiovascular (CV) disease, their relationship to mortality and specific cause of death has not been reported. Methods: Analyses were performed on the first digitally recorded electrocardiogram (ECG) on 43 903 patients at the Palo Alto Veterans Administration Medical Center since 1987. After appropriate exclusions, 40 020 patients remained. Using computerized algorithms, P-wave amplitude and duration in 12 leads as well as several standardized ECG interpretations were extracted. The main outcome measures were pulmonary and CV mortality. Results: During a mean follow-up of 6 years there were 3417 CV and 1213 pulmonary deaths. After adjusting for age and heart rate in a Cox regression model, P-wave amplitude in the inferior leads was the strongest predictor of pulmonary death (hazard ratio [HR]: 3.0, 95% confidence interval [CI]: 2.3-3.9, P < .0001 for an amplitude >2.5 mm), outperforming all other ECG criteria. The depth of P-wave inversion in leads V 1 or V 2 and P-wave duration were strong predictors of CV death (HR: 1.7, 95% CI: 1.5-2.0, P < 0.0001 for a P-wave inversion deeper than 1 mm), outperforming many previously established ECG predictors of CV death. Conclusions: P-wave amplitude in the inferior leads is the strongest independent predictor of pulmonary death while P-wave duration and the depth of P-wave inversion in leads V 1 or V 2 significantly predict CV death. These measurements can be obtained easily and should be considered as part of clinical risk stratification.

Six highly trained marathon runners developed myocardial infarction. One of the two cases of clinically diagnosed myocardial infarction was fatal, and there were four cases of angiographically-proven infarction. Two athletes had significant arterial disease of two major coronary arteries, a third had stenosis of the anterior descending and the fourth of the right coronary artery. All these athletes had warning symptoms. Three of them completed marathon races despite symptoms, one athlete running more than 20 miles after the onset of exertional discomfort to complete the 56 mile Comrades Marathon. In spite of developing chest pain, another athlete who died had continued training for three weeks, including a 40 mile run. Two other athletes also continued to train with chest pain. We conclude that the marathon runners studied were not immune to coronary heart disease, nor to coronary atherosclerosis and that high levels of physical fitness did not guarantee the absence of significant cardiovascular disease. In addition, the relationship of exercise and myocardial infarction was complex because two athletes developed myocardial infarction during marathon running in the absence of complete coronary artery occlusion. We stress that marathon runners, like other sportsmen, should be warned of the serious significance of the development of exertional symptoms. Our conclusions do not reflect on the possible value of exercise in the prevention of coronary heart disease. Rather we refute exaggerated claims that marathon running provides complete immunity from coronary heart disease.

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