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Background: Post-systolic shortening (PSS) has been proposed as a marker of myocardial ischemia. We sought to determine if PSS is associated with coronary artery calcium (CAC) score in patients with suspected stable angina. Methods: We retrospectively studied 522 patients with suspected stable angina pectoris (mean age 60±11 years, 44% male) who underwent speckle tracking echocardiography and assessment of the Agatston CAC score by computed tomography. The post-systolic index (PSI) was defined as follows: [(peak systolic strain - maximum strain in cardiac cycle)/maximum strain in cardiac cycle] x 100. PSS was present if PSI≥20% in one myocardial wall segment. Patients were divided into categories of CAC score: no coronary artery disease (0), minimal (1-10), mild (11-100), moderate (101-400) and severe (>400). We assessed the CAC score continuously using negative binomial regression models for highly dispersed count data, and categorically using Spearman's correlation. Results: Each 1% absolute increase in the PSI was associated with a 7% relative increase in CAC score (95%CI: +0% to +15%, P=0.037, figure 1a), while each wall displaying PSS was associated with a 37% relative increase in CAC score (+8% to +74%, P=0.010, figure 1b). After adjustment for age, sex, hypertension, dyslipidemia and E/A-ratio, both PSI (+10%, 95%CI +1% to +21%, P=0.038) and number of walls with PSS (+60% [+23% to +112%], P<0.001) remained independently associated with the CAC score. Both PSI (Rho 0.12, P=0.006) and walls with PSS (Rho 0.13, P=0.001, figure 1c) increased significantly with increasing categories of CAC score. Conclusion: PSS is independently associated with CAC score in patients with suspected stable angina pectoris and may aid in the identification of patients with an increased CAC score. [ABSTRACT FROM AUTHOR]

Introduction: Patients with type 2 diabetes (T2D) have high levels of epicardial (EAT) and pericardial (PAT) adipose tissue, which due to their intimate proximities to the myocardium, are believed to impact cardiac structure and function in a paracrine manner. EAT is known to secrete inflammatory and sympathetic factors, and apply mechanical stress on the cardiac muscle that could contribute to heart failure. Hypothesis: We hypothesize that EAT and PAT are associated with reduced diastolic and systolic function in a large population of T2D. Methods: 1030 patients with T2D were included in this cross-sectional study. 260 were excluded due to atrial fibrillation (n=62), heart valve disease (n=34) or known ischemic heart disease (n=164). The final study population comprised 770 patients. A comprehensive baseline echocardiography was performed including conventional imaging, tissue Doppler imaging, and 2D speckle tracking. Total cardiac fat (CAT) including EAT and PAT were measured from the parasternal long axis view. Results: 465 (60%) were men, with an age average (SD) of 63±10 years, and known diabetes duration of 12±8 years. Mean total cardiac fat was 11.9±3.6 mm with a mean EAT of 4.6±1.8 mm and mean PAT of 6.3±2.8 mm. Total cardiac fat was associated with measures of decreased diastolic function including peak A velocity (SE) (0.64 cm/s (0.20), p =0.001), lateral E'(-0.13 cm/s (0.03), p <0.001), E/A ratio (-0.01 (0.03), p <0.001), and lateral E/E' (0.13, (0.05), p =0.002). The associations remained after adjusting for age, sex, systolic blood pressure, LDL, HbA1c, and were mainly driven by EAT (all p<0.04 in adjusted models) and not PAT (all p>0.05). Split by the median, patients with high vs. low EAT levels had significantly higher mean E/E'(11.4 (0.25) vs. 10.1 (0.2) p <0.001). In contrast, CAT was only associated with increasing global longitudinal strain (0.08% (0.03) p =0.01), and no other systolic parameters. Conclusion: In patients with T2D, total cardiac adipose tissue was associated with measures of decreased diastolic function primarily driven by epicardial and not pericardial adipose tissue. These results indicate that epicardial and total cardiac adipose tissue may be biomarkers of diastolic dysfunction. [ABSTRACT FROM AUTHOR]

Background: Color Tissue Doppler imaging M-mode through the mitral leaflet is an easy and precise method to obtain the cardiac time intervals including the left ventricular ejection time (LVET). The aim of this study was to investigate whether the LVET can be used to predict cardiovascular morbidity and mortality following acute coronary syndrome (ACS). Methods: We retrospectively studied 390 patients with ACS (mean age 64 ±12 years, men 74%, STEMI 81%, mean LVEF 41±11%, mean LVET 256±35ms) who underwent echocardiography, following percutaneous coronary intervention. The LVET was measured. The primary endpoint was major adverse cardiac events (MACE) and consisted of heart failure, myocardial infarction and cardiovascular death. The secondary endpoint was all-cause mortality. Patients with prevalent HF were excluded. Results: During a median follow-up of 3 years, 180 patients (46%) reached the composite endpoint MACE, and 77 (20%) suffered from all-cause mortality. LVET was significantly associated with risk of MACE (HR 1.13; 95% CI (1.08-1.18), p<0.001) with a 13% increase in risk per 10ms decrease in LVET (figure). The association remained significant after adjusting for age, sex, hypertension, diabetes, body mass index, previous ischemic heart disease, STEMI, multivessel culprit lesions, left ventricular ejection fraction, left ventricular mass index, E/e', E/A and deceleration time (HR 1.10; 95% CI (1.03-1.17), p=0.002 per 10ms decrease). Additionally, the LVET predicted all-cause mortality and the association remained significant even after multivariable adjustment (HR 1.11; 95% CI (1.01-1.21), p=0.032 per 10ms decrease). Conclusion: In patients with ACS the LVET provides novel and independent prognostic information on the risk of cardiovascular morbidity and mortality. [ABSTRACT FROM AUTHOR]