Abstract

Background

The occurrence of atrial fibrillation, circadian fluctuation in blood pressure, and oxygen desaturation at night is likely associated with the pathophysiology of wake-up stroke. Whether patients who experience wake-up strokes are candidates for thrombolysis treatment is a serious dilemma. The aim is to investigate the association between risk factors and wake-up stroke and to determine variations that are associated with the pathophysiology of wake-up stroke.

Methods

Five major electronic databases were searched using a fitted search strategy to identify relevant studies. Odds ratios with 95% CIs were used to calculate estimates, and the Quality Assessment for Diagnostic Accuracy Studies-2 tool was used to conduct the assessment quality.

Results

A total of 29 studies were included in this meta-analysis. Hypertension is not associated with wake-up stroke (odds ratio, 1.14 [95% CI, 0.94–1.37]; P = .18). Atrial fibrillation is an independent risk factor to wake-up stroke, with a statistically significant difference (odds ratio, 1.28 [95% CI, 1.06–1.55]; P = .01). Subgroup analysis showed a different result in patients with sleep-disordered breathing, although no significant difference was assessed.

Conclusion

This study revealed that atrial fibrillation is an independent risk factor for wake-up stroke and that patients with atrial fibrillation who also experience sleep-disordered breathing tend to have fewer wake-up strokes.

Abstract

Background

For patients with non–ST-segment elevation acute coronary syndrome (NSTE-ACS), prasugrel was recommended over ticagrelor in a recent randomized controlled trial, although more data are needed on the rationale. Here, the effects of P2Y12 inhibitors on ischemic and bleeding events in patients with NSTE-ACS were investigated.

Methods

Clinical trials that enrolled patients with NSTE-ACS were included, relevant data were extracted, and a network meta-analysis was performed.

Results

This study included 37,268 patients with NSTE-ACS from 11 studies. There was no significant difference between prasugrel and ticagrelor for any end point, although prasugrel had a higher likelihood of event reduction than ticagrelor for all end points except cardiovascular death. Compared with clopidogrel, prasugrel was associated with decreased risks of major adverse cardiovascular events (MACE) (hazard ratio [HR], 0.84; 95% CI, 0.71–0.99) and myocardial infarction (HR, 0.82; 95% CI, 0.68–0.99) but not an increased risk of major bleeding (HR, 1.30; 95% CI, 0.97–1.74). Similarly, compared with clopidogrel, ticagrelor was associated with a reduced risk of cardiovascular death (HR, 0.79; 95% CI, 0.66–0.94) and an increased risk of major bleeding (HR, 1.33; 95% CI, 1.00–1.77; P = .049). For the primary efficacy end point (MACE), prasugrel showed the highest likelihood of event reduction (P = .97) and was superior to ticagrelor (P = .29) and clopidogrel (P = .24).

Conclusion

Prasugrel and ticagrelor had comparable risks for every end point, although prasugrel had the highest probability of being the best treatment for reducing the primary efficacy end point. This study highlights the need for further studies to investigate optimal P2Y12 inhibitor selection in patients with NSTE-ACS.

Abstract

Background

Left ventricular diastolic dysfunction and nocturnal “nondipping” of blood pressure detected via ambulatory blood pressure monitoring are predictors of increased cardiovascular morbidity.

Methods

A prospective cohort study including normotensive women with a history of preeclampsia in their current pregnancy was conducted. All cases were subjected to 24-hour ambulatory blood pressure monitoring and 2-dimensional transthoracic echocardiography 3 months after delivery.

Results

This study included 128 women with a mean (SD) age of 28.6 (5.1) years and a mean (SD) basal blood pressure of 123.1 (6.4)/74.6 (5.9) mm Hg. Among the participants, 90 (70.3%) exhibited an ambulatory blood pressure monitoring profile illustrating nocturnal blood pressure “dipping” (the mean night to day time blood pressure ratio ≤ 0.9), whereas 38 (29.7%) were nondippers. Diastolic dysfunction (impaired left ventricular relaxation) was present in 28 nondippers (73.7%), whereas none of the dippers exhibited diastolic dysfunction. Women with severe preeclampsia were more frequently nondippers (35.5% vs 24.2%; P = .02) and experienced diastolic dysfunction (29% vs 15%; P = .01) than were those with mild preeclampsia. Severe preeclampsia (odds ratio [OR], 1.08; 95% CI, 1.05–10.56; P < .001) and history of recurrent preeclampsia (OR, 1.36; 95% CI, 1.3–4.26; P ≤ .001) were significant predictors for nondipping status and diastolic dysfunction (OR, 1.55; 95% CI, 1.1–2.2; and OR, 1.23; 95% CI, 1.2–2.2, respectively; P < .05).

Conclusion

Women with a history of preeclampsia were at higher risk for developing late cardiovascular events. The severity and recurrence of preeclampsia were significant predictors of both nondipping profile and diastolic dysfunction.

Abbreviations and Acronyms

BiVP: biventricular pacing
CRT: cardiac resynchronization therapy
CSP: conduction system pacing
HF: heart failure
HisBP: His bundle pacing
LBBP: left bundle branch pacing
LVEF: left ventricular ejection fraction
RCT: randomized controlled trial

Introduction

Cardiac resynchronization therapy (CRT) is an established therapy for medically refractory heart failure (HF), with a reduction in hospitalization and mortality in addition to improved cardiac function and functional capacity shown in landmark clinical trials.^1,2 Cardiac resynchronization therapy is also indicated for patients with systolic dysfunction requiring frequent ventricular pacing (>40%) to prevent deleterious remodeling and cardiomyopathy associated with ventricular

Abbreviations and Acronyms

CABG: coronary artery bypass grafting
CPB: cardiopulmonary bypass
GDMT: guideline-directed medical therapy
HR: hazard ratio
IABP: intra-aortic balloon pump
LCOS: low cardiac output syndrome
LV: left ventricular
LVEF: left ventricular ejection fraction
STICH: Surgical Treatment for Ischemic Heart Failure

Introduction

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