Association between time to reperfusion and echocardiography assessed left ventricular filling pressure in patients with first ST-segment elevation myocardial infarction undergoing primary coronary intervention

  Background: Diastolic dysfunction and elevated left ventricular (LV) filling pressure fol­lowing acute myocardial infarction are associated with adverse outcomes. Although time to reperfusion is a powerful prognostic marker following acute myocardial infarction, little is known about its impact on diastolic function and LV filling pressure. We hypothesized that delayed time to reperfusion will be associated with worse diastolic function. Methods: This study included 180 consecutive patients with first ST elevation myocardial in­farction (STEMI) treated by primary percutaneous coronary intervention (PCI). They presen­ted of chest pain within 24 h and underwent echocardiography within 3 days of primary PCI. Results: Median time to reperfusion, defined as the time from symptom onset to reperfusion at the end of primary PCI, was 185 min (interquartile range 120–660). Patients with reperfu­sion time > 185 min (n = 92) had a significantly higher E/septal e’ (13.3 ± 5.0 vs. 9.7 ± 2.3, p < 0.001) and E/lateral e’ (9.8 ± 3.5 vs. 7.8 ± 2.2, p < 0.001) ratios, and more advanced diastolic grade (p < 0.001) compared to those having early reperfusion (n = 88). There were no significant differences in LV ejection fraction and left atrial volume between the two groups. Time to reperfusion was an independent predictor of early E/average e’ ratio. The adverse ef­fect of late reperfusion on diastolic dysfunction was more prominent in patients with anterior myocardial infarction. Conclusions: Longer time to reperfusion is associated with early elevated LV diastolic pres­sure in primary PCI-treated patients with STEMI.

Elevated resting heart rate is associated with the metabolic syndrome

<p>Abstract</p> <p>Background</p> <p>Increased resting heart rate (RHR) may be associated with increased cardiovascular morbidity. Our aim was to explore the possibility that increased RHR is associated with the prevalence of the metabolic syndrome (MetS) in a sample of apparently healthy individuals and those with cardiovascular risk factors.</p> <p>Methods</p> <p>We performed a cross-sectional analysis in a large sample of apparently healthy individuals who attended a general health screening program and agreed to participate in our survey. We analyzed a sample of 7706 individuals (5106 men and 2600 women) with 13.2% of men and 8.9% of the women fulfilling the criteria for the MetS. The participants were divided into quintiles of resting heart rate. Multiple adjusted odds ratio was calculated for having the MetS in each quintile compared to the first.</p> <p>Results</p> <p>The multi-adjusted odds for the presence of the MetS increased gradually from an arbitrarily defined figure of 1.0 in the lowest RHR quintile (<60 beats per minute (BPM) in men and <64 BPM in women) to 4.1 and 4.2 in men and women respectively in the highest one (≥80 BPM in men and ≥82 BPM in women).</p> <p>Conclusion</p> <p>Raised resting heart rate is significantly associated with the presence of MetS in a group of apparently healthy individuals and those with an atherothrombotic risk. The strength of this association supports the potential presence of one or more shared pathophysiological mechanisms for both RHR and the MetS.</p

Waist circumference as the predominant contributor to the micro-inflammatory response in the metabolic syndrome: a cross sectional study

<p>Abstract</p> <p>Background</p> <p>The metabolic syndrome (MetS) is associated with the presence of low grade inflammation. Our aim was to analyze the inter-relations between each of the components of the metabolic syndrome (MetS) and four inflammatory markers, namely high sensitivity C-reactive protein (hs-CRP), the erythrocyte sedimentation rate, the concentration of fibrinogen and the white blood cell count.</p> <p>Methods</p> <p>We have analyzed data collected between September 2002 and June 2009 in the Tel-Aviv medical center inflammation survey (TAMCIS). We recruited both apparently healthy individuals and individuals presenting with atherothrombotic risk factors. All participants were enrolled during their routine annual health check-up and gave their written informed consent. This is a cross sectional study in which we have fitted linear regression models using inflammatory markers as the dependant variables and adjust them according to the different components of the MetS and multiple other confounders.</p> <p>Results</p> <p>Included were 12,072 individuals of whom there were 7,760 men at a mean (S.D.) age of 44 (11) years, and 4,312 women aged 44 (11) years. A significant correlation was noted between most components of the MetS and all inflammatory markers, the most significant one being with hs-CRP. In the multi-adjusted regression analysis, waist was the factor that best explained the variability of hs-CRP, in both women and men. It also remained a significant variable for the other inflammatory markers.</p> <p>Conclusions</p> <p>From amongst the various components of the MetS, waist circumference appears to exert the most influence upon the presence and intensity of the micro-inflammatory response.</p

The multi-modality cardiac imaging approach to the Athlete's heart: an expert consensus of the European Association of Cardiovascular Imaging

The term 'athlete's heart' refers to a clinical picture characterized by a slow heart rate and enlargement of the heart. A multi-modality imaging approach to the athlete's heart aims to differentiate physiological changes due to intensive training in the athlete's heart from serious cardiac diseases with similar morphological features. Imaging assessment of the athlete's heart should begin with a thorough echocardiographic examination. Left ventricular (LV) wall thickness by echocardiography can contribute to the distinction between athlete's LV hypertrophy and hypertrophic cardiomyopathy (HCM). LV end-diastolic diameter becomes larger (>55 mm) than the normal limits only in end-stage HCM patients when the LV ejection fraction is <50%. Patients with HCM also show early impairment of LV diastolic function, whereas athletes have normal diastolic function. When echocardiography cannot provide a clear differential diagnosis, cardiac magnetic resonance (CMR) imaging should be performed. With CMR, accurate morphological and functional assessment can be made. Tissue characterization by late gadolinium enhancement may show a distinctive, non-ischaemic pattern in HCM and a variety of other myocardial conditions such as idiopathic dilated cardiomyopathy or myocarditis. The work-up of athletes with suspected coronary artery disease should start with an exercise ECG. In athletes with inconclusive exercise ECG results, exercise stress echocardiography should be considered. Nuclear cardiology techniques, coronary cardiac tomography (CCT) and/or CMR may be performed in selected cases. Owing to radiation exposure and the young age of most athletes, the use of CCT and nuclear cardiology techniques should be restricted to athletes with unclear stress echocardiography or CMR

Cardiac Screening of Young Athletes: a Practical Approach to Sudden Cardiac Death Prevention.

PURPOSE OF REVIEW: We aim to report on the current status of cardiovascular screening of athletes worldwide and review the up-to-date evidence for its efficacy in reducing sudden cardiac death in young athletes. RECENT FINDINGS: A large proportion of sudden cardiac death in young individuals and athletes occurs during rest with sudden arrhythmic death syndrome being recognised as the leading cause. The international recommendations for ECG interpretation have reduced the false-positive ECG rate to 3% and reduced the cost of screening by 25% without compromising the sensitivity to identify serious disease. There are some quality control issues that have been recently identified including the necessity for further training to guide physicians involved in screening young athletes. Improvements in our understanding of young sudden cardiac death and ECG interpretation guideline modification to further differentiate physiological ECG patterns from those that may represent underlying disease have significantly improved the efficacy of screening to levels that may make screening more attractive and feasible to sporting organisations as a complementary strategy to increased availability of automated external defibrillators to reduce the overall burden of young sudden cardiac death

Associations between outdoor temperature and markers of inflammation: a cohort study

<p>Abstract</p> <p>Background</p> <p>Associations between ambient temperature and cardiovascular mortality are well established. This study investigated whether inflammation could be part of the mechanism leading to temperature-related cardiovascular deaths.</p> <p>Methods</p> <p>The study population consisted of a cohort of 673 men with mean age of 74.6 years, living in the greater Boston area. They were seen for examination roughly every 4 years, and blood samples for inflammation marker analyses were drawn in 2000-2008 (total of 1254 visits). We used a mixed effects model to estimate the associations between ambient temperature and a variety of inflammation markers (C-reactive protein, white blood cell count, soluble Vascular Cell Adhesion Molecule-1, soluble Intercellular Adhesion Molecule-1, tumor necrosis factor alpha, and interleukins -1β, -6 and -8). Random intercept for each subject and several possible confounders, including combustion-related air pollution and ozone, were used in the models.</p> <p>Results</p> <p>We found a 0 to 1 day lagged and up to 4 weeks cumulative responses in C-reactive protein in association with temperature. We observed a 24.9% increase [95% Confidence interval (CI): 7.36, 45.2] in C-reactive protein for a 5°C decrease in the 4 weeks' moving average of temperature. We observed similar associations also between temperature and soluble Intercellular Adhesion Molecule-1 (4.52%, 95% CI: 1.05, 8.10, over 4 weeks' moving average), and between temperature and soluble Vascular Cell Adhesion Molecule-1 (6.60%, 95% CI: 1.31, 12.2 over 4 weeks' moving average). Penalized spline models showed no deviation from linearity. There were no associations between temperature and other inflammation markers.</p> <p>Conclusions</p> <p>Cumulative exposure to decreased temperature is associated with an increase in inflammation marker levels among elderly men. This suggests that inflammation markers are part of intermediate processes, which may lead to cold-, but not heat-, related cardiovascular deaths.</p