Jonathan G. Schwartz

Long-Term Marathon Running Is Associated with Low Coronary Plaque Formation in Women

Introduction Marathon running is presumed to improve cardiovascular risk, but health benefits of high volume running are unknown. High-resolution coronary computed tomography angiography and cardiac risk factor assessment were completed in women with long-term marathon running histories to compare to sedentary women with similar risk factors. Methods Women who had run at least one marathon per year for 10–25 yr underwent coronary computed tomography angiography, 12-lead ECG, blood pressure and heart rate measurement, lipid panel, and a demographic/health risk factor survey. Sedentary matched controls were derived from a contemporaneous clinical study database. CT scans were analyzed for calcified and noncalcified plaque prevalence, volume, stenosis severity, and calcium score. Results Women marathon runners (n = 26), age 42–82 yr, with combined 1217 marathons (average 47) exhibited significantly lower coronary plaque prevalence and less calcific plaque volume. The marathon runners also had less risk factors (smoking, hypertension, and hyperlipidemia); significantly lower resting heart rate, body weight, body mass index, and triglyceride levels; and higher high-density lipoprotein cholesterol levels compared with controls (n = 28). The five women runners with coronary plaque had run marathons for more years and were on average 12 yr older (65 vs 53) than the runners without plaque. Conclusion Women marathon runners had minimal coronary artery calcium counts, lower coronary artery plaque prevalence, and less calcified plaque volume compared with sedentary women. Developing coronary artery plaque in long-term women marathon runners appears related to older age and more cardiac risk factors, although the runners with coronary artery plaque had accumulated significantly more years running marathons.

Fifty Men, 3510 Marathons, Cardiac Risk Factors, and Coronary Artery Calcium Scores

Introduction/Purpose Many male marathon runners have elevated coronary artery calcium (CAC) scores despite high physical activity. We examined the association between CAC scores, cardiovascular risk factors, and lifestyle habits in long-term marathoners. Methods We recruited men who had run one or more marathons annually for 25 consecutive years. CAC was assessed using coronary computed tomography angiography. Atherosclerotic cardiovascular disease risk factors were measured with a 12-lead ECG, serum lipid panel, height, weight, resting blood pressure and heart rate, and a risk factor questionnaire. Results Fifty males, mean age 59 ± 0.9 yr with a combined total of 3510 marathons (median = 58.5, range = 27–171), had a mean BMI of 22.44 ± 0.4 kg·m−2, HDL and LDL cholesterols of 58 ± 1.6 and 112 ± 3.7 mg·dL−1, and CAC scores from 0 to 3153. CAC scores varied from 0 in 16 runners to 1–100 in 12, 101–400 in 12, and >400 in 10. There was no statistical difference in the number of marathons run between the four groups. Compared with marathoners with no CAC, marathoners with moderate and extensive CAC were older (P = 0.002), started running at an older age (P = 0.003), were older when they ran their first marathon (P = 0.006), and had more CAD risk factors (P = 0.005), and marathoners with more CAC had higher rates of previous tobacco use (P = 0.002) and prevalence of hyperlipidemia (P = 0.01). Conclusion Among experienced males who have run marathons for 26–34 yr and completed between 27 and 171 marathons, CAC score is related to CAD risk factors and not the number of marathons run or years of running. This suggests that among long-term marathoners, more endurance exercise is not associated with an increased risk of CAC.

Myocardial Bridge and Acute Plaque Rupture

A myocardial bridge (MB) is a common anatomic variant, most frequently located in the left anterior descending coronary artery, where a portion of the coronary artery is covered by myocardium. Importantly, MBs are known to result in a proximal atherosclerotic lesion. It has recently been postulated that these lesions predispose patients to acute coronary events, even in cases of otherwise low-risk patients. One such mechanism may involve acute plaque rupture. In this article, we report 2 cases of patients with MBs who presented with acute coronary syndromes despite having low cardiovascular risk. Their presentation was life-risking and both were treated urgently and studied with coronary angiographies and intravascular ultrasound. This latter modality confirmed a rupture of an atherosclerotic plaque proximal to the MB as a likely cause of the acute events. These cases, of unexplained acute coronary syndrome in low-risk patients, raise the question of alternative processes leading to the event and the role MB play as an underlying cause of ruptured plaques. In some cases, an active investigation for this entity may be warranted, due to the prognostic implications of the different therapeutic modalities, should an MB be discovered.

The right atrium and tricuspid annulus are cardinal structures in tricuspid regurgitation with or without pulmonary hypertension

BACKGROUND Right heart structural abnormalities occur in both tricuspid regurgitation (TR) and pulmonary hypertension (PH). They may occur independently or together, but their joint effects on cardiac structure are incompletely described. This study examined the interactions of TR severity and PH on right heart structural changes. METHODS The study evaluated 455 patients undergoing both echocardiography and CT angiography (CTA). Cases were divided into 3 groups by TR severity: trace (n=217), mild (n=174), and significant (moderate or severe, n=64). Each TR level was subdivided into two groups by PH absent or present. Cardiac structural measurements included tricuspid annulus area (TAA), right atrial (RA) and right ventricular volume (RV) indexed to body surface area. RESULTS Analysis by TR and PH showed that indexed RA Volume and TAA were very sensitive to TR severity. RA volume was most affected by pulmonary hypertension when TR was trace or mild, while PH had less effect on TAA. In significant TR, neither RA volume nor TAA were changed by PH. Indexed RV volume was insensitive to trace and mild TR, and PH similarly had little effect. CONCLUSIONS RA volume and tricuspid annulus area enlarge in proportion to TR severity, trace through significant. PH impacts RA volume but only in trace and mild TR. RA volume best reflects TR impact on right heart structure, both with and without PH. Right atrial volume and tricuspid annulus area are the cardinal indices of TR-induced right heart structural disease et al.l severities. ULTRAMINI ABSTRACT Right heart structural effects of TR and PH were examined in this study. Patients were evaluated by echo and CTA, and grouped by TR severity as trace, mild, and significant, and were subdivided by PH absence/presence. Analysis by TR severity and PH showed that Indexed RA volume is the parameter most sensitive to TR severity, and PH causes incremental RA volume increases in trace/mild TR. Indexed tricuspid annulus area (TAA) similarly increases with TR severity, but was unaffected by PH at any TR severity. RV volume is insensitive to TR severity and PH. Indexed right atrial volume and tricuspid annulus area are cardinal indices for TR-induced right heart structural disease and increase proportionally to TR severity. RA volume is more sensitive to PH than is tricuspid annular area. TR severity may be more accurately assessed by increased RA volume and annulus area. PERSPECTIVE STATEMENT The right atrium (RA) and tricuspid annulus (TA) are the cardinal cardiac structures affected by tricuspid regurgitation (TR). They each enlarge with TR severity. The right ventricle exhibits minimal change across TR severity. Pulmonary hypertension (PH) enhances TR-mediated RA and TA dilation, but only in trace and mild TR. PH has no effect on RA, TA, or RV size in significant TR. CENTRAL MESSAGE Right atrial volume and tricuspid annulus area are the most sensitive to TR severity, and are also sensitive to pulmonary hypertension.

Invasive physiologic and anatomic multimodality assessment of myocardial bridging.

A 61-year-old man was referred with 9 years of exertional chest pain. He described daily episodes of sharp, substernal chest pain, associated with shortness of breath and extreme fatigue. His symptoms were progressive, despite both β and calcium channel blockade, and he was no longer able to perform