Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. It places an enormous burden on the patients, caregivers, and the society at large. While the main themes in the care of an AF patient have not changed over the years and continue to focus on stroke prevention, control of the ventricular, rate and rhythm maintenance, there have been a number of new developments in each of these realms. This paper will discuss the "hot" topics in AF in 2012 including new and upcoming medical and invasive management strategies for this condition.
The pathogenesis of takotsubo syndrome (TS) has not been established yet. The literature data dealing with the pathogenesis of TS are abundant but scattered among different medical specialities. Subarachnoid hemorrhage and other acute intracranial diseases and injuries are among the important and currently well-recognized trigger factors for TS. In both induced and spontaneous subarachnoid hemorrhages, signs suggestive of increased cardiac sympathetic overactivity have been documented. Surgical and pharmacological sympathectomy has shown to have protective cardiac effects in both animal and human studies. Increase in local release of norepinephrine from the heart of patients with TS has been measured. Signs of both cardiac sympathetic denervation and myocardial lesions adjacent to the cardiac nerve terminals have been seen. Furthermore, the systematized and typically circumferential pattern of ventricular wall motion abnormality is incongruent with the coronary artery supply region and appears most likely to follow the cardiac sympathetic nerve distribution. In conclusion, compelling literature data support the hypothesis that acute cardiac sympathetic disruption and norepinephrine seethe and spillover is causing TS in predisposed patients. TS is most probably an acute cardiac sympathetic disease entity causing myocardial stunning in which takotsubo is one among other cardiac image study findings.
This study proposes a method for ventricular late potentials (VLPs) detection using time-frequency representation and wavelet denoising in high-resolution electrocardiography (HRECG). The analysis is performed both with the signal averaged electrocardiography (SAECG) and in real time. A comparison between the temporal and the time-frequency analysis is also reported. In the first analysis the standard parameters QRSd, LAS40, and RMS40 were used; in the second normalized energy in time-frequency domain was calculated. The algorithm was tested adding artificial VLPs to real ECGs.
Objective. Studies have shown that inflammation plays an important role in pathogenesis of coronary artery disease. The present study was designed to evaluate the role of high WBC count before CABG in predicting the risk of ischemic events after CABG. Methods and Results. This prospective study was carried out on 380 patients who underwent CABG surgery. Ninety seven patients (25.5%) had recurrent ischemic event. Mean WBC count before CABG surgery in patients with recurrent ischemic event was 7267 mic/lit ± 1863, which was significantly higher than the others, with a mean WBC count of 6721 mic/lit ± 1734 (P = 0.011). Patients with a WBC count more than 6000 mic/lit were at the highest risk for recurrent ischemic event (OR = 2.11, 95% CI = 1.18-3.44, P = 0.009). After adjustment for age, sex, family history, smoking, hyperlipidemia, Logestic Euro score, post opretive enzyme release (CK.mb), arterial graft and BMI, the relationship between the group with WBC count higher than 6000 mic/lit and recurrent of ischemic event remained significant (OR = 2.25, 95% CI = 1.2 to 4, P = 0.005). Conclusions. High WBC count before CABG surgery is an independent risk factor for ischemic events one year after the surgery.
Hyperglycemia, which occurs in the perioperative period during cardiac surgery, has been shown to be associated with increased morbidity and mortality. The management of perioperative hyperglycemia during coronary artery bypass graft surgery and all cardiac surgical procedures has been the focus of intensive study in recent years. This report will paper the pathophysiology responsible for the detrimental effects of perioperative hyperglycemia during cardiac surgery, show how continuous insulin infusions in the perioperative period have improved outcomes, and discuss the results of trials designed to determine what level of a glycemic control is necessary to achieve optimal clinical outcomes.
Although MRI is widely used to diagnose stenotic carotid arteries, it also detects characteristics of the atherosclerotic plaque itself, including its size, composition, and activity. These features are emerging as additional risk factors for stroke that can be feasibly acquired clinically. This paper summarizes the state of evidence for a clinical role for MRI of carotid atherosclerosis.
The aim of this study is to analyze MMP-2 and sTNF-R1 variability, potent predictors of cardiovascular events, in stable hypertensive patients during a 12-month followup. 234 asymptomatic patients (age 60 ± 13, 136 male) out of 252 patients with essential hypertension were followed up. MMP-2 and sTNF-R1 were measured at baseline and after 12 months (stage I). To compare MMP-2 and sTNF-R1 levels over time interval, we used the statistical method of Bland-Altman. MMP-2 and sTNF-R1 reproducibility was good in our patients for the two intervals with a coefficient of reproducibility of 8.2% and 11.3%, respectively. The percentages of patients within 1.96 × standard deviation of the mean were 93.6% and 92.7%. An elevated coefficient of correlation was obtained for MMP-2, basal versus stage I (r = 0.55, P < 0.0001) and for sTNF-R1 (r = 0.75, P < 0.0001). There is good stability in MMP-2 and sTNF-R1 levels in a followup study of patients with stable hypertension. As a consequence, assessment of its concentrations may be a useful tool for monitoring the follow-up of these patients. Measured variations in MMP-2 and sTNF-R1 levels, exceeding 8.2% and 11.3%, respectively, may indicate an increase in cardiovascular risk, thus, could be used to optimizing treatment than blood pressure control alone.
Metabolic syndrome increases the risk of all-cause mortality, cardiovascular mortality and cardiovascular events in patients with cardiovascular disease (CVD). This study assessed the predictors of metabolic syndrome, both its incidence and resolution in a cohort of cardiac rehabilitation program graduates. Methods. A total of 154 and 80 participants without and with metabolic syndrome respectively were followed for 48 months. Anthropometric measurements, metabolic risk factors, and quality of life were assessed at baseline and at 48 months. Logistic regression models were used to assess the predictors of metabolic syndrome onset and resolution. Results. Increasing waist circumference (OR 1.175, P ≤ 0.001) was an independent predictor for incident metabolic syndrome (R(2) for model = 0.46). Increasing waist circumference (OR 1.234, P ≤ 0.001), decreasing HDL-C (OR 0.027, P = 0.005), and increasing triglycerides (OR 3.005, P = 0.003) were predictors of metabolic syndrome resolution. Conclusion. Patients with CVD that further develop metabolic syndrome are particularly susceptible for the cascade of cardiovascular events and mortality. Increasing waist circumference confers a higher risk for future onset of metabolic syndrome in this group of patients. They will require closer follow-up and should be targeted for further prevention strategies after cardiac rehabilitation program completion.
Purpose. To provide an ovine model of ventricular remodeling and reverse remodeling by creating congestive heart failure (CHF) and then treating it by implanting a left ventricular assist device (LVAD). Methods. We induced volume-overload heart failure in 2 sheep; 20 weeks later, we implanted an LVAD and assessed recovery 11 weeks thereafter. We examined changes in histologic and hemodynamic data and levels of cellular markers of CHF. Results. After CHF induction, we found increases in LV end-diastolic pressure, LV systolic and diastolic dimensions, wall thickness, left atrial diameter, and atrial natriuretic protein (ANP) and endothelin-1 (ET-1) levels; β-adrenergic receptor (BAR) and dystrophin expression decreased markedly. Biopsies confirmed LV remodeling. After LVAD support, LV systolic and diastolic dimensions, wall thickness, and mass, and ANP and ET-1 levels decreased. Histopathologic and hemodynamic markers improved, and BAR and dystrophin expression normalized. Conclusions. We describe a successful sheep model for ventricular and reverse remodeling.