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Aims Angina and no obstructive coronary artery disease (ANOCA) is common. A potential cause of angina in this patient population is a myocardial bridge (MB). We aimed to study the anatomical and haemodynamic characteristics of an MB in patients with ANOCA. Methods and results Using intravascular ultrasound (IVUS), we identified 184 MBs in 154 patients. We evaluated MB length, arterial compression, and halo thickness. MB muscle index (MMI) was defined as MB length×halo thickness. Haemodynamic testing of the MB was performed using an intracoronary pressure/Doppler flow wire at rest and during dobutamine stress. We defined an abnormal diastolic fractional flow reserve (dFFR) as ≤0.76 during stress. The median MB length was 22.9 mm, arterial compression 30.9%, and halo thickness 0.5 mm. The median MMI was 12.1. Endothelial and microvascular dysfunction were present in 85.4% and 22.1%, respectively. At peak dobutamine stress, 94.2% of patients had a dFFR ≤0.76 within and/or distal to the MB. MMI was associated with an abnormal dFFR. Conclusions In select patients with ANOCA who have an MB by IVUS, the majority have evidence of a haemodynamically significant dFFR during dobutamine stress, suggesting the MB as being a cause of their angina. A comprehensive invasive assessment of such patients during coronary angiography provides important diagnostic information that can guide management.

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.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.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.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.

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.

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.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.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, HDL and LDL cholesterols of 58 ± 1.6 and 112 ± 3.7 mg·dL, and CAC scores from 0 to 3153. CAC scores varied from 0 in 16 runners to 1-100 in 12, 101-400 in 12, and400 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).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.

Microvascular obstruction (MVO) remains a major problem in acute coronary syndromes and has potent impact on both short- and long-term prognosis. No clinical trials to date show efficacy against MVO. Because of these clinical trial failures, this study evaluated a multi-modal therapeutic approach to

Invasive evaluation and treatment of coronary artery disease (CAD) has traditionally been based upon coronary angiography to determine the need for and the success of revascularization. However, coronary angiography augmented with fractional flow reserve (FFR) creates a paradigm shift, providing a more complete functional assessment of coronary lesions. Measuring FFR to identify ischemic lesions and guide revascularization results in fewer adverse outcomes, including persistent angina, myocardial infarction, and mortality. An ischemic lesion identified by FFR is more likely to lead to adverse events when compared with an angiographically similar lesion with nonischemic FFR when both are treated medically. Although the mechanism explaining this is unclear, it is likely multifactorial, including the impact of mechanical forces, upregulation of inflammatory mediators, and the amount of distal myocardial tissue at risk. Using both anatomic and ischemia-guided assessments (such as the Functional SYNTAX Score) aids in the therapeutic decision-making process in patients with multivessel CAD. This review focuses on the evidence for FFR-guided management of multivessel CAD.

Objectives To determine outcomes following balloon aortic valvuloplasty (BAV) in aortic stenosis (AS) patients with a left ventricular ejection fraction (LVEF)

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.

Coronary microvascular dysfunction during STEMI is poorly understood. Dynamic microvascular resistance (dMVR) can now be measured precisely and in real time using controlled coronary flow infusion, a simple catheter-based technique. This study characterized infarct zone microvascular dysfunction

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

To determine outcomes following balloon aortic valvuloplasty (BAV) in aortic stenosis (AS) patients with a left ventricular ejection fraction (LVEF)20%.Severe AS patients with a LVEF20% are excluded from United States (U.S.) transcatheter aortic valve replacement (TAVR) trials and often surgical aortic valve replacement (AVR). The role for BAV to enhance LVEF is unclear.Our BAV database of 270 consecutive patients extending from 2005 through 2010 was queried for a preoperative LVEF20%. Demographics, echocardiograms, procedural technique, and outcomes were analyzed. Pre- and postoperative echocardiograms were used to determine improvement in aortic valve area (AVA) and LVEF.Sixteen patients were identified with a median age of 82 years. The composite Society of Thoracic Surgeons' (STS) mortality risk was 16.4%. The median preoperative AVA and LVEF were 0.60 cm(2) and 16%, respectively, and postoperative AVA and LVEF were 0.77 cm(2) and LVEF 19%, respectively. About 15 of the 16 patients had postoperative echocardiograms available for comparison. And 7 of these 15 (47%) demonstrated improvement in LVEF to ≥20% (median LVEF 25%). The absence of coronary disease and improvement in AVA of ≥0.2 cm(2) was associated with postoperative LVEF of ≥20%. Procedural mortality was 0%. The 30-day, 6-month, and 1-year survival was 69%, 56%, and 29%. STS's mortality risk score ≥15% was associated with short-term mortality.With appropriate technique, BAV can be reasonably safe in patients with LVEF20%. Roughly half of these patients demonstrated improvement in LVEF to ≥20%.

Imaging modalities utilized in the interventional cardiology suite have seen an impressive evolution and expansion recently, particularly with regard to the recent interest in three-dimensional (3D) imaging. Despite this, the backbone of visualization in the catheterization laboratory remains two-dimensional (2D) X-ray fluoroscopy and cine-angiography. New imaging techniques under development, referred to as three-dimensional rotational angiography (RA) and C-arm CT, hold great promise for improving current device implantation and understanding of cardiovascular anatomy. This paper reviews the evolution of rotational angiography and advanced 3D X-ray imaging applications to interventional cardiology.

Angiographic studies of ST-elevation myocardial infarction (STEMI) show that occlusive thrombi occur in coronary arteries within the proximal third of each major vessel, within about 35 mm from the ostium. These findings suggest that these high-risk regions are sites of plaque vulnerability. Multidetector CTA (MDCTA) visualizes not only lumen but also calcified and uncalcified coronary plaque. We therefore studied the distribution of coronary plaque in patients to determine plaque distribution to compare result with location of angiographic myocardial infarction thrombus. Methods: 48 outpatients (mean age 57 +− 5) undergoing Dual Source MDCTA (asymptomatic or with atypical symptoms) were studied. Most distal plaque location was measured for ostial-termination distance and composition (calcified/noncalcified) determined by one expert observer using validated, commercial plaque characterization software for lesion location and lesion length. Results: Location of the most distal plaque was as follows, LAD (n=35) 31.8 mm, LCX (n=21) 33.0 mm, and RCA (n=24) 56.0 mm. Mean lesion lengths were LAD 19.4 +− 13.4 mm, LCX 15.1 +− 9.6 and RCA 18.4 +− 9.8 mm. Mean volume (cu mm) for calcified and noncalcified plaque was 130 +− 176 and 204 +− 249 respectively, for a ratio of 0.64. There was no propensity of either calcified or uncalcified plaque to aggregate longitudinally in the arteries. Conclusions: The distribution and location of coronary artery plaque by MDCTA identically matches the known location of coronary artery vulnerability determined by angiographic studies. This finding suggests that STEMI does not occur in distal coronary locations simply because little plaque occurs in these areas. Calcified plaque volume measured in 3-dimensions underestimates total plaque volume by a factor of 2.6. Calcific plaque is thus the ‘tip of the iceberg’.