Head to head comparisons of two modalities of perfusion adenosine stress echocardiography with simultaneous SPECT

<p>Abstract</p> <p>Background</p> <p>Real-time perfusion (RTP) contrast echocardiography can be used during adenosine stress echocardiography (ASE) to evaluate myocardial ischemia. We compared two different types of RTP power modulation techniques, angiomode (AM) and high-resolution grayscale (HR), with ^99mTc-tetrofosmin single-photon emission computed tomography (SPECT) for the detection of myocardial ischemia.</p> <p>Methods</p> <p>Patients with known or suspected coronary artery disease (CAD), admitted to SPECT, were prospectively invited to participate. Patients underwent RTP imaging (SONOS 5500) using AM and HR during Sonovue^®infusion, before and throughout the adenosine stress, also used for SPECT. Analysis of myocardial perfusion and wall motion by RTP-ASE were done for AM and HR at different time points, blinded to one another and to SPECT. Each segment was attributed to one of the three main coronary vessel areas of interest.</p> <p>Results</p> <p>In 50 patients, 150 coronary areas were analyzed by SPECT and RTP-ASE AM and HR. SPECT showed evidence of ischemia in 13 out of 50 patients. There was no significant difference between AM and HR in detecting ischemia (p = 0.08). The agreement for AM and HR, compared to SPECT, was 93% and 96%, with Kappa values of 0.67 and 0.75, respectively (p < 0.001).</p> <p>Conclusion</p> <p>There was no significant difference between AM and HR in correctly detecting myocardial ischemia as judged by SPECT. This suggests that different types of RTP modalities give comparable data during RTP-ASE in patients with known or suspected CAD.</p

Quantitative detection of myocardial ischaemia by stress echocardiography; a comparison with SPECT

<p>Abstract</p> <p>Aims</p> <p>Real-time perfusion (RTP) adenosine stress echocardiography (ASE) can be used to visually evaluate myocardial ischaemia. The RTP power modulation technique angio-mode (AM), provides images for off-line perfusion quantification using Qontrast^®software, generating values of peak signal intensity (A), myocardial blood flow velocity (β) and myocardial blood flow (Axβ). By comparing rest and stress values, their respective reserve values (A-r, β-r, Axβ-r) are generated. We evaluated myocardial ischaemia by RTP-ASE Qontrast^®quantification, compared to visual perfusion evaluation with ^99mTc-tetrofosmin single-photon emission computed tomography (SPECT).</p> <p>Methods and Results</p> <p>Patients admitted to SPECT underwent RTP-ASE (SONOS 5500) using AM during Sonovue^®infusion, before and throughout adenosine stress, also used for SPECT. Visual myocardial perfusion and wall motion analysis, and Qontrast^®quantification, were blindly compared to one another and to SPECT, at different time points off-line.</p> <p>We analyzed 201 coronary territories (left anterior descendent [LAD], left circumflex [LCx] and right coronary [RCA] artery territories) in 67 patients. SPECT showed ischaemia in 18 patients and 19 territories. Receiver operator characteristics and kappa values showed significant agreement with SPECT only for β-r and Axβ-r in all segments: area under the curve 0.678 and 0.665; P < 0.001 and < 0.01, respectively. The closest agreements were seen in the LAD territory: kappa 0.442 for both β-r and Axβ-r; P < 0.01. Visual evaluation of ischaemia showed good agreement with SPECT: accuracy 93%; kappa 0.67; P < 0.001; without non-interpretable territories.</p> <p>Conclusion</p> <p>In this agreement study with SPECT, RTP-ASE Qontrast^®quantification of myocardial ischaemia was less accurate and less feasible than visual evaluation and needs further development to be clinically useful.</p

Psychological stress and risk of incident atrial fibrillation in men and women with known atrial fibrillation genetic risk scores

Psychological stress has been reported as a possible trigger of atrial fibrillation (AF). No studies have investigated whether any association between stress and AF could be modified by genetic susceptibility to AF (AF-genetic risk score (AF-GRS)). 8765 men and 13,543 women from the Malmö Diet Cancer Study, a population-based cohort, were included in the analyses. A variable representing stress was constructed from questions measuring job strain, and from one question assessing non-occupational stress. Cox proportional hazards regression models were adjusted for known covariates of AF. Mean follow-up times and number of recorded incident AF were 14.2 years and 1116 events for men, and 15.1 years and 932 events for women. Among women, high stress was associated with AF in the age adjusted model (hazard ratio [HR], 1.22; 95% confidence interval [CI], 1.01-1.47) but not following multivariable adjustment (HR, 1.15; 95% CI, 0.95-1.39). Stress was not associated with incident AF in men. AF-GRS was significantly associated with incident AF for both genders. Stress did not interact significantly with genetic susceptibility to AF in men or women. Chronic stress is not associated with long-term incident hospital diagnosed AF. This association does not appear to be modified by genetic susceptibility to AF

Concentration of BNP, endothelin 1, pro-inflammatory cytokines (TNF-alpha, IL-6) and exercise capacity in patients with heart failure treated with carvedilol

Background: Recent studies on the pathophysiology of heart failure indicate the role of neurohormones and immune and inflammatory processes as potential mechanisms involved in the pathogenesis and clinical course of chronic heart failure (CHF). Aim: To analyse the relationship between concentrations of brain natriuretic peptide (BNP), endothelin-1 (ET-1), inflammatory cytokines (TNF-alpha, IL-6) and cardiopulmonary stress test parameters, and to evaluate their changes during carvedilol treatment. Methods: The study included 86 patients (81 men and 5 women) aged from 35 to 70 years (56.8 +/- 9.19) with symptomatic heart failure and left ventricular ejection fraction < 40%, receiving an inhibitor of angiotensin II converting enzyme, diuretic and/or digoxin but not beta-blockers. All patients at baseline, and then at 3 and 12 months after treatment, underwent a panel of studies to assess functional capacity according to NYHA, echocardiographic and cardiopulmonary stress test (CPX) parameters, and serum concentrations of BNP, ET-1, TNF-alpha and IL-6. Before introducing carvedilol we found a weak relationship between concentrations of BNP, ET-1, IL-6 and decreased VO2 (peak). Results: At 12 months exercise tolerance was significantly improved (exercise stress testing prolonged by 143.9 s, p=0.001) and an increase in metabolic equivalent (MET) by 1.41 (p=0.001) was observed. The VO2 (peak) was nonsignificantly increased by a mean of 0.9 ml/kg/min. In patients with baseline VO2 (peak) < 14 ml/kg/min the concentrations of ET-1 and TNF-alpha were significantly higher than in the remaining ones, and after treatment they were significantly reduced. In these patients VO2 (peak)%N was also significantly increased (39.5 +/- 7.5 vs. 50.1 +/- 15,0; p=0.013). The number of patients with VO2 (peak) < 14 ml/kg/min also significantly decreased from 39 to 21 (p=0.013). Conclusions: In patients with HF decreased value of VO2 (peak) is associated with LV systolic function disorders and increased levels of BNP, ET-1, TNF-alpha and IL-6. Chronic treatment with carvedilol improves LV systolic function, exercise tolerance and peak oxygen consumption and is associated with significant decrease of BNP, ET-1, TNF-alpha and IL-6 concentrations

Cox proportional hazards regression models for the effect of interaction between psychological stress and quartiles of coronary artery disease (CAD) genetic risk score (GRS) on incident CAD, fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death.

<p>Cox proportional hazards regression models for the effect of interaction between psychological stress and quartiles of coronary artery disease (CAD) genetic risk score (GRS) on incident CAD, fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death.</p

Baseline characteristics according to Genetic Risk Score (GRS) Quartiles and psychological stress.

<p>Baseline characteristics according to Genetic Risk Score (GRS) Quartiles and psychological stress.</p

Sudden cardiac death risk factors in patients with heart failure treated with carvedilol

Background: Chronic heart failure (CHF) is associated with a high risk of sudden cardiac death (SCID). Most frequently SCID occurs in patients with NYHA class II and III. Aim: To evaluate the influence of prolonged carvedilol therapy on SCID risk in CHF patients. Methods: The study included 86 patients (81 men and 5 women) aged 56.8 +/- 9.19 (35-70) years with CHF in NYHA class II and III receiving an ACE inhibitor and diuretics but not beta-blockers. At baseline and after 12 months of carvedilol therapy the following risk factors for SCID were analysed: in angiography - occluded infarct-related artery; in echocardiography - left ventricular ejection fraction (LVEF) 140 ml; in ECG at rest - sinus heart rate (HRs) > 75/min, sustained atrial fibrillation, increased QTc; in 24-hour ECG recording - complex arrhythmia, blunted heart rate variability (SDNN 114 ms. The analysis of SCD risk factors in basic examination in patients who suddenly died was also performed. Results: During one-year carvedilol therapy heart transplantation was performed in 2 patients; 5 patients died. At 12 months the following risk factors for SCID were significantly changed: HRs > 75/min (50 vs. 16 patients, p=0.006), LVEF < 30% (37 vs. 14 patients, p=0.01), SDNN < 100 ms (19 vs. 9 patients, p=0.04). At 12 months the number of risk factors for SCD in each patient was significantly reduced (p=0.001). In patients who suddenly died we found a greater amount of SCID risk factors in basic examination (7 vs. 5) as compared to alive patients. Conclusions: Prolonged beta-adrenergic blockade reduces risk of sudden cardiac death through significant LVEF increase, reduction of HR at rest and improvement of HRV