Search

The optimal technique for bifurcation of left main coronary artery (LMCA) stenting has been a subject of controversy since the inception of drug-eluting stents. We searched PubMed, Clinical Trials Registry, and the Cochrane Central Register of Controlled Trials from January 2002 through October 2021. A total of 13 studies comparing the use of provisional versus dual stenting in patients with LMCA bifurcation lesions were included. Any major adverse cardiac event (MACE) was considered the primary composite end point. The secondary end points included individual components of MACE, including death, myocardial infarction, and target lesion revascularization. The treatment effect was defined as the log odds ratio (OR) of provisional over dual stenting for cumulative event rate at 3 years. In 12 studies with 8,377 patients included for MACE, the use of a provisional-stenting strategy was associated with a significant reduction of 3-year MACE (OR 0.64, 95% confidence interval [CI] 0.46 to 0.88) compared with a dual-stenting strategy, primarily driven by target lesion revascularization (OR 0.51, 95% CI 0.36 to 0.73). No significant difference was found regarding death (OR 0.88; 95% CI 0.65 to 1.21) or myocardial infarction (OR 0.97, 95% Cl 0.61 to 1.54). In conclusion, our meta-analysis suggests that provisional stenting should be the preferred technique over dual stenting when treating LMCA bifurcation lesions with drug-eluting stents. Further randomized controlled studies compounded with intracoronary imaging comparing the 2 strategies are warranted.

Epidemiological studies have established the association between excessive alcohol consumption and systemic hypertension (SH). However, there are conflicting reports of the association of low to moderate alcohol consumption with SH. The objective of the study was to examine the associations of alcohol consumption and blood pressure categories using the 2017 American College of Cardiology/American Heart Association high blood pressure guidelines. This analysis included 17,059 participants from the Third National Health and Nutrition Examination Survey. Alcohol consumption was ascertained by way of a questionnaire. Blood pressure (mm Hg) was measured during the in-home interview and the participant's visit to the mobile examination center. We used multivariable logistic regression models to examine cross-sectional associations of alcohol consumption and blood pressure categories based on new American College of Cardiology/American Heart Association High Blood Pressure guidelines. Models were adjusted for age, gender, income, and cardiovascular risk factors. Compared with never drinkers, moderate drinkers (7 to 13 drinks/week) had increased odds of prevalent stage 1 and stage 2 SH (odds ratio [95% confidence interval] 1.51 [1.22 to 1.87] and 1.55 [1.20 to 2.00]). Similarly, there were significantly higher odds of prevalent stage 1 and stage 2 SH among heavy drinkers (≥14 drinks/week) (odds ratio [95% confidence interval] 1.65 [1.33 to 2.05] and 2.46 [1.93 to 3.14]). We did not find any association between alcohol consumption and elevated blood pressure category. Response bias must be considered because alcohol consumption was self-reported. Our study indicates the need for further research to understand the potential mechanisms by which alcohol consumption increases the risk of SH. In conclusion, this analysis from a population-based survey showed an association between moderate and heavy alcohol consumption and a higher prevalence of SH.

Resting heart rate (RHR) is independently associated with cardiovascular disease (CVD) risk. We determined whether RHR, measured in mid-life, is also associated with cognitive decline. We studied 13,720 middle-aged white and black ARIC participants without a history of stroke or atrial fibrillation. RHR was obtained from a 12-lead resting electrocardiogram at the baseline visit (1990 to 1992) and categorized into groups as60 (reference), 60 to 69, 70 to 79 and ≥80 beats/min. Cognitive scores were obtained at baseline and at up to 2 additional visits (1996 to 1998 and 2011 to 2013). The primary outcome was a global composite cognitive score (Z-score) derived from 3 tests: delayed word recall, digit symbol substitution, and word fluency. The associations of RHR with cognitive decline and incident dementia were examined using linear mixed-effects and Cox hazard models, respectively, adjusting for sociodemographics, CVD risk factors, and AV-nodal blockade use. Multiple imputation methods were used to account for attrition over follow-up. Participants had mean ± SD age of 58 ± 6 years; 56% were women, 24% black. Average RHR was 66 ± 10 beats/min. Over a mean follow-up of 20 years, those with RHR ≥80 beats/min had greater global cognitive decline (average adjusted Z-score difference -0.12 [95% confidence interval -0.21, -0.03]) and increased risk for incident dementia (hazard ratio 1.28 (1.04, 1.57), compared with those with RHR60 beats/min. In conclusion, elevated RHR is independently associated with greater cognitive decline and incident dementia over 20 years. Further studies are needed to determine whether the associations are causal or secondary to another underlying process, and whether modification of RHR can affect cognitive decline.

Autonomic nervous system (ANS) dysfunction plays a role in atrial fibrillation (AF) initiation. Cardiorespiratory fitness modulates ANS function and is inversely associated with resting heart rate (RHR) and risk of AF. Thus, we sought to study the association between RHR, as a surrogate for ANS function, and incident AF independent of exercise capacity (EC). We analyzed 51,436 subjects without previous AF who underwent a clinically indicated exercise stress test. Incident AF was ascertained through claims files. RHR was measured before stress testing, and EC was estimated by peak metabolic equivalents of task. We studied the association between RHR categories (70, 70 to 85 [reference], and85 beats/min) and incident AF using Cox models adjusted for risk factors and for EC. We tested for interaction between RHR and age, gender, smoking, and EC. Mean (SD) age was 53 (13) years, 53% were men, and 28% were black. Participants with RHR70 beats/min were older, more likely to be men, have higher EC, and more likely to smoke but less likely to have diabetes and hypertension. Over a median of 5.5 years, RHR70 beats/min was associated with 14% increased risk of AF (95 CI 6% to 25%) in fully adjusted models, whereas RHR85 beats/min was not associated with AF risk after adjusting for EC. Results for RHR analyzed continuously and by quartile were similar. No interaction was seen. In conclusion, subjects with low RHR at all levels of EC are at increased risk of AF and may benefit from heart rhythm surveillance, particularly in the presence of other AF risk factors.

Whether resting heart rate (RHR) predicts mortality independent of fitness is not well established, particularly among women. We analyzed data from 56,634 subjects (49% women) without known coronary artery disease or atrial fibrillation who underwent a clinically indicated exercise stress test. Baseline RHR was divided into 5 groups with60 beats/min as reference. The Social Security Death Index was used to ascertain vital status. Cox hazard models were performed to determine the association of RHR with all-cause mortality, major adverse cardiovascular events, myocardial infarction, or revascularization after sequential adjustment for demographics, cardiovascular disease risk factors, medications, and fitness (metabolic equivalents). The mean age was 53 ± 12 years and mean RHR was 73 ± 12 beats/min. More than half of the participants were referred for chest pain; 81% completed an adequate stress test and mean metabolic equivalents achieved was 9.2 ± 3. There were 6,255 deaths over 11.0-year mean follow-up. There was an increased risk of all-cause mortality with increasing RHR (p trend0.001). Compared with the lowest RHR group, participants with an RHR ≥90 beats/min had a significantly increased risk of mortality even after adjustment for fitness (hazard ratio 1.22, 95% confidence interval 1.10 to 1.35). This relationship remained significant for men, but not significant for women after adjustment for fitness (p interaction0.001). No significant associations were seen for men or women with major adverse cardiovascular events, myocardial infarction, or revascularization after accounting for fitness. In conclusion, after adjustment for fitness, elevated RHR was an independent risk factor for all-cause mortality in men but not women, suggesting gender differences in the utility of RHR for risk stratification.

Arterial calcification reflects an atherosclerotic process associated with vascular stiffness. Whether baseline coronary artery calcium (CAC) and extra-coronary calcium (ECC), measured using noncontrast computed tomography imaging, are associated with incident hypertension is poorly understood. We studied participants from the Multi-Ethnic Study of Atherosclerosis without measured or self-reported hypertension at baseline. Incident hypertension was defined by blood pressure criteria (BP, ≥140/90 mmHg), BP medication use, or both, and was assessed at in-person visits. We analyzed incident hypertension using multivariable-adjusted discrete-time proportional hazards models. Net reclassification improvement (NRI) assessed whether CAC reclassified hypertension risk when added to the Framingham hypertension risk score. Among 3,304 subjects analyzed, mean age was 59 ± 10 years; 48% were male and 42% were white. There were 1,283 incident hypertension cases over a median (interquartile range) follow-up time of 10.6 (4.5, 11.5) years. Each 1-unit increase in ln(CAC+1) was independently associated with a 12% higher risk of hypertension (95% confidence interval [CI] 9% to 16%). Relative to CAC = 0, patients with CAC >400 had a hazard ratio for incident hypertension of 2.2 (95% CI 1.8 to 2.9). There was no interaction by age, gender, or baseline BP (p = 0.43, 0.19, 0.09, respectively). Continuous NRI analyses demonstrated that CAC can reclassify risk of incident hypertension; NRI = 0.19 (95% CI 0.10 to 0.26). Furthermore, all measurements of ECC were significantly associated with incident hypertension, even after adjustment for CAC (hazard ratios ranging from 1.36 to 1.38). In conclusion, patients with CAC and ECC are at markedly higher risk of incident hypertension and may benefit from more intensified prevention efforts.