Sex-Specific Cardiometabolic Determinants of Postoperative Atrial Fibrillation After Cardiac Surgery.

BACKGROUND: Cardiometabolic diseases increase the risk of postoperative atrial fibrillation (POAF), a complication leading to higher long-term risk of major cardiovascular events (MACE). It remains unknown whether the effect of these risk factors differs according to sex. We sought to evaluate the sex-specific predictors of POAF after coronary artery bypass grafting (CABG). METHODS: In a prospective registry of patients undergoing isolated CABG, we compared predictors of POAF between sexes with logistic regression models. Because of high prevalence of abdominal obesity in women, > 80% having a waist circumference (WC) ≥ 88 cm, median WC values were used to define abdominal obesity (men ≥ 102 cm, women ≥ 100 cm). RESULTS: This analysis included 6177 individuals (17% women). Mean age was 65.6 ± 8.9 years. POAF occurred in 32% of men and 28% of women (P < 0.05). Compared with men, women with POAF had similar WC; higher prevalence of hypertension and diabetes; lower high-density lipoprotein (HDL)-cholesterol; and higher glucose, triglyceride, low- density lipoprotein (LDL)-cholesterol, and C-reactive protein levels (all P < 0.05). After adjustment, age and abdominal obesity were associated with POAF in both sexes (P < 0.05). The interaction of WC with sex suggested a worse impact of WC on POAF risk among women (adjusted odds ratio [OR], 1.97; 95% confidence interval [CI], 1.48-2.62 vs in men 1.33; 95% CI, 1.17-1.50; P for interaction = 0.01). CONCLUSIONS: Abdominal obesity is a major predictor of POAF in both sexes, with higher risk in women. These results emphasize the need for enhanced strategies to manage abdominal obesity and its cardiometabolic consequences in the general population and the potential to develop sex-specific preventive interventions to reduce risk of POAF.

Arterial Health After Preeclampsia: Role of Chronic Hypertension in the Early Vascular Aging (EVA) Study.

BACKGROUND: Preeclampsia (PE) is associated with increased cardiovascular risk. Recent data have shown worse left ventricular remodeling and diastolic function in women with PE and persistent hypertension (HTN). We performed a comprehensive arterial hemodynamic assessment to evaluate the contribution of persistent HTN on arterial health after PE. METHODS: We recruited 40 women with PE history and 40 age-matched controls (6 months to 6 years postpartum). We evaluated arterial hemodynamics with validated techniques combining applanation tonometry and transthoracic echocardiography, comparing three groups: previous PE with persistent HTN (PE-HTN), previous PE with normalized blood pressure (PE-noHTN) and controls, using multivariable linear regression adjusted for age, body surface area, heart rate, diabetes, smoking history, creatinine, and gravidity. RESULTS: Eight (20%) of the post-PE women had persistent HTN. Mean age was 35.8 ±â€…3.9 years, median number of pregnancies was 2 (range 1-7), and time since last pregnancy 2.1 (range 0.5-5.7) years (not different between groups, P > 0.05). Compared to controls and to PE-noHTN, PE-HTN had higher aortic stiffness, wave reflections, pulsatile, and steady arterial load (P < 0.05 for each). Among PE-noHTN, aortic stiffness, wave reflections and steady arterial load were worse than controls (P < 0.05 for each), with smaller effect sizes. CONCLUSIONS: This is the most comprehensive assessment of arterial hemodynamics and first to demonstrate the contribution of persistent HTN on worse arterial health following PE. Since measures of arterial health are associated with cardiovascular events in the population, the combination of previous PE and chronic HTN may represent a higher risk subgroup who could benefit from targeted prevention strategies.

Sex-specific correlates of valvular and arterial calcification burden in patients with moderate aortic stenosis.

INTRODUCTION: There are significant sex differences in the prevalence and severity of cardiac calcifying processes. Women harbour more severe mitral annular calcification (MAC), while men exhibit worse aortic valve (AVC) and coronary artery (CAC) calcification. To better understand these differences, we investigated the correlates of cardiac calcification according to sex. METHODS: We conducted a cross-sectional study of 406 patients with ≥mild aortic stenosis (AS) defined by an aortic valve area ≤1.5 cm2, a peak aortic jet velocity >2.0 m/s, or a mean transvalvular gradient >15 mm Hg. Doppler-echocardiography and non-contrast multidetector CT were performed concomitantly to assess AS and cardiac calcifications. RESULTS: Mean age was 71±11 years and 33% were women. The AS haemodynamics were not significantly different between sexes (all p>0.50), with a mean indexed aortic valve area of 0.59±0.21 cm2/m2, peak aortic jet velocity of 2.78 (2.37-3.68) m/s, and mean gradient of 17.9 (12.8-31.3) mm Hg for the whole cohort. Compared with men, women harboured lower AVC (480 (222-1191) vs 1003 (484-2329) Agatston unit, AU; p<0.0001) and CAC (366 (50-914) vs 618 (167-1357) AU; p=0.007), but more severe MAC (60 (1-887) vs 48 (0-351) AU; p=0.08) and ascending aorta calcification (227 (43-863) vs 142 (7-493) AU; p=0.03). After comprehensive adjustment, sex remained an independent predictor of each cardiac calcification subtype (all p<0.02) except for the ascending aorta (p=0.32). In multivariable analysis, certain variables, like age or bicuspid aortic valve, were associated with the calcification scores in both sexes. Sex-specific predictors of calcification burden were absence of angiotensin receptor blockers (ß=-0.26; p=0.007) and renal impairment (ß=0.26; p=0.003) for AVC, and bisphosphonates (ß=0.20; p=0.05) for CAC in women; coronary artery disease (ß=0.25; p=0.001) for AVC, and angiotensin receptor blockers (ß=0.19; p=0.02) and calcium/vitamin D (ß=0.15; p=0.02) for MAC in men. CONCLUSION: In AS, factors associated with cardiac valvular and arterial calcification differ between sexes, suggesting an important contributory role of sex in the pathophysiology of these calcifying processes.

Effects of Cyproheptadine on Mitral Valve Remodeling and Regurgitation After Myocardial Infarction.

BACKGROUND: Ischemic mitral regurgitation (MR) is primarily caused by left ventricle deformation, but leaflet thickening with fibrotic changes are also observed in the valve. Increased levels of 5-hydroxytryptamine (5-HT; ie, serotonin) are described after myocardial infarction (MI); 5-HT can induce valve fibrosis through the 5-HT type 2B receptor (5-HT2BR). OBJECTIVES: This study aims to test the hypothesis that post-MI treatment with cyproheptadine (5-HT2BR antagonist) can prevent ischemic MR by reducing the effect of serotonin on mitral biology. METHODS: Thirty-six sheep were divided into 2 groups: inferior MI and inferior MI treated with cyproheptadine (0.5 mg/kg/d). Animals were followed for 90 days. Blood 5-HT, infarct size, left ventricular volume and function, MR fraction and mitral leaflet size were assessed. In a complementary in vitro study, valvular interstitial cells were exposed to pre-MI and post-MI serum collected from the experimental animals. RESULTS: Increased 5-HT levels were observed after MI in nontreated animals, but not in the group treated with cyproheptadine. Infarct size was similar in both groups (11 ± 3 g vs 9 ± 5 g; P = 0.414). At 90 days, MR fraction was 16% ± 7% in the MI group vs 2% ± 6% in the cyproheptadine group (P = 0.0001). The increase in leaflet size following MI was larger in the cyproheptadine group (+40% ± 9% vs +22% ± 12%; P = 0.001). Mitral interstitial cells overexpressed extracellular matrix genes when treated with post-MI serum, but not when exposed to post-MI serum collected from treated animals. CONCLUSIONS: Cyproheptadine given after inferior MI reduces post-MI 5-HT levels, prevents valvular fibrotic remodeling, is associated with larger increase in mitral valve size and less MR.

Secondary prevention after CABG: do new agents change the paradigm?

PURPOSE OF REVIEW: Coronary artery bypass graft (CABG) surgery remains the gold-standard treatment for multivessel and left main coronary artery disease. Despite significant improvement in cardiovascular outcomes, patients undergoing CABG remain at risk for recurrent adverse ischemic events and other cardiovascular outcomes (coronary revascularisation, stroke, cardiac death, etc.). The purpose of this review is to summarize the most recent evidence in pharmacological preventive therapies addressing the residual cardiovascular risk in patients who have undergone CABG. RECENT FINDINGS: Novel cardiovascular pharmacological preventive strategies targeting inflammatory, metabolic and prothrombotic (antiplatelet and anticoagulation) pathways have been recently assessed, with promising results for secondary prevention after CABG. SUMMARY: Secondary prevention is an essential part of postoperative care after CABG. Novel lipid-lowering and glucose-controlling agents suggest a strong and consistent benefit on native coronary artery disease and overall cardiovascular outcomes. The role and the choice of enhanced antiplatelet/anticoagulation/lipid/glucose-modulating therapies following CABG should be better defined and deserves further investigation. Additional studies are required to identify new therapeutic target addressing the specific multifactorial nature of the graft CV disease and identifying the best preventive strategies for long-term graft patency.

A Paralyzing Case of Myalgias.

BACKGROUND Myalgia, which describes muscle pain or soreness, is a common presenting complaint encountered in the Emergency Department, in inpatient settings and in outpatient settings. Its differential diagnosis is broad and includes benign as well as more serious clinical entities. Some of the common causes of myalgias include viral infections, strenuous exercise, and medications. Succinylcholine is a well-known neuromuscular blockade agent that is frequently used for rapid sequence intubation and short surgeries. CASE REPORT We present the case of a 70-year-old male who presented to the Emergency Department with a chief complaint of acute, severe onset diffuse myalgia leading to the inability to mobilize. He was being investigated for recent onset generalized lymphadenopathy and had undergone a diagnostic lymph node biopsy under general anesthesia 2 days prior to his presentation. He was diagnosed with presumed succinylcholine-induced myalgias after other etiologies were deemed less likely with thorough history, physical examination, and laboratory investigations. Succinylcholine binds nicotinic acetylcholine receptors of the neuromuscular junction and produces prolonged depolarization during which activation of the muscle is blocked. Initial depolarization of the neuromuscular junction induces hectic fasciculation of the muscle fibers, which in turn may be responsible for the occurrence of post-operative myalgias (POM). This entity can be severe and debilitating and is self-limited. CONCLUSIONS Succinylcholine remains a commonly used agent in anesthesia and succinylcholine-induced myalgia should remain in the differential diagnosis of acute, non-inflammatory myalgia. Its recognition can help avoid unwarranted, possibly invasive investigations and their associated additional healthcare costs.