Zero fluoroscopy approach versus fluoroscopy approach for cardiac arrhythmia ablations: A systematic review and meta-analysis.

BACKGROUND: Radiofrequency catheter ablation for cardiac arrhythmias has traditionally been guided by fluoroscopy. Fluoroscopy exposes the patient, operator, and staff to ionizing radiation which has no safe dose void of stochastic and deterministic biologic risks. Zero fluoroscopy (ZF) approaches for catheter ablation have been advocated to eliminate these risks. We conducted a meta-analysis comparing acute procedure success, recurrence-free survival, complications, and procedure times between the approaches. METHODS: We conducted a literature search from inception through December 2020 in the databases of EMBASE and MEDLINE. We included randomized controlled trials and cohorts that compared the outcomes of interest in ZF and conventional/low fluoroscopy (CF/LF) approaches. The outcomes sought were acute procedure success, recurrence-free survival, complications, and procedure times. Effect estimates were combined, using the random-effects, generic inverse variance method of DerSimonian and Laird. RESULTS: Sixteen studies from 2013 to 2020, including 6052 patients (2219 ZF, 3833 CF/LF) were included. There were no significant differences in acute procedure success rate (odds ratio [OR]: 1.10, 95% confidence interval [CI]: 0.75-1.59), recurrence-free survival (OR: 1.08, 95% CI: 0.78-1.49), periprocedural complication rate (OR: 0.72, 95% CI: 0.45-1.16), or total procedure time (weighted mean difference 2.32 min, 95% CI: -2.85-7.50) between ZF and CF/LF approaches, respectively. Overall, only 1.26% of patients crossed over from ZF to CF/LF arm. CONCLUSIONS: Periprocedural and postprocedural outcomes with a ZF approach compared favorably with traditional fluoroscopic guidance without increasing procedural times. As comfort with ZF grows, coupled with evolving mapping technologies, this method has potential to become the standard approach for catheter ablation.

Toward Brief Dual Antiplatelet Therapy and P2Y12 Inhibitors for Monotherapy After PCI.

The optimal duration of dual antiplatelet therapy (DAPT) after percutaneous coronary intervention remains a controversial topic. The European Society of Cardiology and the American College of Cardiology/American Heart Association recommend at least 6 and 12 months of DAPT after PCI in patients with stable coronary artery disease or acute coronary syndrome, respectively. Although prolonging DAPT duration reduces ischemic events, it is associated with higher rates of bleeding and possible fatal outcomes. The DAPT score can be an important tool to identify patients who may still benefit from prolonged therapy. Nevertheless, several recent randomized controlled trials showed that shortening DAPT duration from 12 to 1-3 months reduces bleeding rates without significantly increasing ischemic event rates. These trials also suggested replacing acetylsalicylic acid (aspirin) with P2Y12 inhibitors after short-term DAPT. We review and compare past and present studies regarding DAPT and analyze the evidence favoring a short DAPT duration and the long-term single antiplatelet agent of choice.

Weight Reduction for Obesity-Induced Heart Failure with Preserved Ejection Fraction.

PURPOSE OF REVIEW: Heart failure with preserved ejection fraction mainly affects the elderly. The obesity phenotype of heart failure with preserved ejection fraction reflects the coexistence of two highly prevalent conditions in the elderly. Obesity may also lead to heart failure with preserved ejection fraction in middle-aged persons, especially in African American women. RECENT FINDINGS: Obesity is twice as common in middle-aged than in elderly persons with heart failure with preserved ejection fraction. Obese middle-aged persons with heart failure with preserved ejection fraction are less likely to be Caucasian and to have atrial fibrillation or chronic kidney disease as comorbidities than elderly patients with heart failure with preserved ejection fraction. Obesity-associated low-grade systemic inflammation may induce/heighten inflammatory activation of the coronary microvascular endothelium, leading to cardiomyocyte hypertrophy/ stiffness, myocardial fibrosis, and left ventricular diastolic dysfunction. Both substantial weight reduction with bariatric surgery and lesser levels of weight reduction with caloric restriction are promising therapeutic approaches to obesity-induced heart failure with preserved ejection fraction.

Bariatric Surgery and Hospitalization for Heart Failure in Morbidly Obese Patients.

BACKGROUND: Bariatric surgery may improve heart failure outcome in morbidly obese patients. However, the safety of bariatric surgery has not been investigated in morbidly obese patients hospitalized for heart failure. We evaluated the effects of bariatric surgery on parameters of hospitalization for heart failure in morbidly obese patients. METHODS: We analyzed administrative discharge data of morbidly obese patients with heart failure as a primary diagnosis. Propensity score matching was performed to assess parameters of hospitalization in morbidly obese patients with and without a history of bariatric surgery. The discharges with diastolic heart failure codes were analyzed separately. RESULTS: Morbid obesity was coded in 4.4% of all discharges. Heart failure was the primary diagnosis in 6.0% of discharges with morbid obesity codes. Only 1% of discharges with morbid obesity and heart failure as primary diagnosis codes were coded for bariatric surgery. Length of stay (p < 0.001), in-hospital mortality (p < 0.001), and the estimated cost of hospitalizations (p < 0.007) were lower in discharges with than without bariatric surgery codes. Length of stay was shorter and in-hospital mortality was lower in discharges with codes for diastolic heart failure and bariatric surgery than with codes for only diastolic heart failure (p < 0.042 and p < 0.001 respectively). CONCLUSION: When hospitalized for heart failure, morbidly obese patients who underwent bariatric surgery fare as well as or slightly better than their counterparts who did not.

Obesity, Hypertension, and Bariatric Surgery.

PURPOSE OF REVIEW: Obesity increases the risk of hypertension. However, blood pressure decreases before any significant loss of body weight after bariatric surgery. We review the mechanisms of the temporal dissociation between blood pressure and body weight after bariatric surgery. RECENT FINDINGS: Restrictive and bypass bariatric surgery lower blood pressure and plasma leptin levels within days of the procedure in both hypertensive and normotensive morbidly obese patients. Rapidly decreasing plasma leptin levels and minimal loss of body weight point to reduced sympathetic nervous system activity as the underlying mechanism of rapid blood pressure decline after bariatric surgery. After the early rapid decline, blood pressure does not decrease further in patients who, while still obese, experience a steady loss of body weight for the subsequent 12 months. The divergent effects of bariatric surgery on blood pressure and body weight query the role of excess body weight in the pathobiology of the obesity phenotype of hypertension. The decrease in blood pressure after bariatric surgery is moderate and independent of body weight. The lack of temporal relationship between blood pressure reduction and loss of body weight for 12 months after sleeve gastrectomy questions the nature of the mechanisms underlying obesity-associated hypertension.

Towards a Saphenous Vein Graft Moratorium.

Atherosclerosis develops and rapidly progresses in saphenous veins grafts after coronary bypass surgery. In contrast to native coronary artery, percutaneous revascularization does not impede the progression of saphenous vein atherosclerosis and saphenous vein graft failure commonly ensues. The protracted patency of arterial grafts is likely to account for most of the long-term superiority of coronary artery bypass surgery over percutaneous revascularization in patients with complex coronary artery disease. Long-lasting, complete coronary revascularization may be best achieved by combining surgical arterial grafting of diseased coronary arteries to percutaneous revascularization with drug-eluting stents than by the continued use of saphenous vein grafts.

A Practical Approach to Hybrid Coronary Revascularization.

Combined surgical and percutaneous coronary revascularization, ie, hybrid coronary revascularization (HCR) consists of surgical left internal mammary artery (LIMA) bypass to the left anterior descending artery (LAD) and percutaneous revascularization of other diseased coronary arteries. Developed as a 1-stage procedure, HCR has not been widely adopted by the cardiovascular community. The recommended minimally invasive approach through a small left thoracotomy incision is technically demanding, and same-day percutaneous revascularization requires a hybrid operating room that is not available in most hospitals. In this review, we consider present HCR protocols, barriers to widespread adoption of HCR, and we give special attention to the surgical approach for the LIMA graft to the LAD and the timing of percutaneous revascularization. We conclude that grafting the LIMA to the LAD through a median sternotomy approach and delaying the percutaneous revascularization may facilitate the widespread use of HCR in patients with multivessel coronary artery disease and a low to intermediate Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery score.

Precardiogenic Shock: A New Clinical Entity.

The pathogenesis of cardiogenic shock (CS) has evolved from an acute event due to a large myocardial infarction to a semiacute event due to rapid hemodynamic deterioration on a background of preexisting left ventricular systolic dysfunction. Pre-CS refers to the period of rapid hemodynamic deterioration that precedes overt CS with hypotension, inflammatory response, and end-organ failure. Mortality remains extremely high in CS and has not improved over the past decades. Pre-CS offers a unique opportunity to initiate early treatment that may result in better clinical outcomes. The present review addresses the definition, recognition, and management of pre-CS with the pharmacologic or mechanical support of the failing left ventricle.

Epicardial Adipose Tissue and Cardiovascular Disease.

PURPOSE OF REVIEW: Epicardial adipose tissue has been associated with the development/progression of cardiovascular disease. We appraise the strength of the association between epicardial adipose tissue and development/progression of cardiovascular diseases like coronary artery disease, atrial fibrillation, and heart failure with preserved ejection fraction. RECENT FINDINGS: Cross-sectional clinical and translational correlative studies have established an association between epicardial adipose tissue and progression of coronary artery disease. Recent studies question this association and underline the need for longitudinal studies. Epicardial adipose tissue also plays a definite role in the pathobiology of atrial fibrillation and its recurrence after ablation. In contrast to an early paradigm, epicardial adipose tissue does not appear to play a key role in the pathogenesis of heart failure with preserved ejection fraction in obese patients. The association of epicardial adipose tissue with atrial fibrillation is robust. In contrast, the association of epicardial adipose tissue with coronary artery disease and heart failure with preserved ejection fraction is tenuous. Additional research, including longitudinal studies, is needed to confirm or refute these proposed associations.

Obesity and Pulmonary Hypertension.

PURPOSE OF REVIEW: Whether the present obesity epidemic will increase the prevalence of pulmonary hypertension over the next decades is unclear. We review the obesity-related mechanisms that may further the development and progression of pulmonary hypertension. RECENT FINDINGS: Systemic and local inflammation, insulin resistance and oxidative stress contribute to the pathobiology of obesity and pulmonary arterial hypertension. Preliminary data suggest that expansion of adipose tissue surrounding the pulmonary artery may hasten the progression of pulmonary arterial hypertension in obese persons. Further, obesity-associated cardiac and pulmonary conditions may increase the prevalence of groups 2 and 3 pulmonary hypertension. The obesity epidemic is likely to increase the prevalence of pulmonary arterial hypertension by enabling vascular remodeling. Obesity-associated cardiac and pulmonary conditions will increase pulmonary hypertension prevalence.