Prophylactic use of carvedilol in patients receiving ANT may protect both systolic and diastolic functions of the left ventricle.

BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.

No abstract

We evaluated the association of total bilirubin with post-percutaneous coronary intervention (PCI) coronary blood flow and in-hospital major adverse cardiac events (MACEs) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. A total of 536 consecutive patients with STEMI (male 79%, mean age = 59.9 ± 12.6 years) admitted within 6 hours from symptom onset were enrolled. Patients were divided into 2 groups based on the thrombolysis in myocardial infarction (MI) flow grade. In-stent thrombosis, nonfatal MI, and in-hospital mortality were significantly higher in no-reflow group (P = .007, P = .002, and P < .001, respectively). On multivariate regression, the total bilirubin levels remained independent predictors of no-reflow (odds ratio [OR] 1.586, 95% confidence interval [CI] 1.02-2.47; P = .042) and in-hospital MACE (OR 1.399, 95% CI 1.053-1.857; P = .020). Serum bilirubin levels were independently associated with no-reflow and in-hospital MACE in patients with STEMI undergoing primary PCI.

Doppler tissue imaging (DTI) has been proposed as a tool for the evaluation of diastolic function. Controversy exists regarding whether DTI measurements are influenced by preload. Changes in the circulating volume associated with hemodialysis result in preload reduction. To determine the influence of preload reduction on DTI and standard pulsed-Doppler transmitral diastolic velocities, 30 patients (mean age 41 +/- 14) with chronic renal insufficiency without overt heart disease were studied by DTI and standard pulsed Doppler before and after hemodialysis. From the apical window, DTI sample volume was placed at the lateral and septal mitral annulus and at the midsegment of lateral and septal myocardial wall of the left ventricle. Peak early diastolic annular and myocardial, and peak late diastolic annular and myocardial velocities were measured. Transmitral peak early and late diastolic velocities were also recorded by standard pulsed Doppler. The peak velocity of early diastolic mitral flow decreased from 100 +/- 30 to 85 +/- 34 cm/s (P < 0.001) after hemodialysis. Hemodialysis elicited marked reduction in early diastolic lateral mitral annular and midlateral myocardial velocities (6.9 +/- 3.2 to 6.3 +/- 2.9 cm/s, P < 0.04 and 6.7 +/- 0.3 to 5.5 +/- 2 cm/s, P < 0.001, respectively). Early diastolic, septal mitral annular, and midseptal myocardial velocities were also significantly decreased (5.8 +/- 2.8 to 4.6 +/- 2 cm/s, P < 0.006 and 6.2 +/- 2 to 5.1 +/- 1 cm/s, P < 0.008, respectively). Late diastolic mitral annular and myocardial velocities did not change. It is concluded that early diastolic mitral annular and myocardial velocities are affected by acute preload reduction. It is necessary to consider preload when diastolic function is assessed by DTI.

Our results suggest that MPV, a determinant of platelet activation, has a positively correlation with blood pressure and elevated in non-dipper compared with dippers and controls. Increased platelet activation could contribute to increase the atherosclerotic risk in non-dipper patients compared with dippers.

No abstract

The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 +/- 0.6 in the COPD group and 2.1 +/- 0.7 in the control group (P = 0.004). The mean Extent score was 37 +/- 16 in the COPD group and 23 +/- 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 +/- 6.3 vs 6.6 +/- 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682-9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023-13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.