Perspectives on Secondary Mitral Regurgitation in Heart Failure.

PURPOSE OF THE REVIEW: This review focuses on broader perspectives of mitral regurgitation (MR) in patients with heart failure. RECENT FINDINGS: The ratio of regurgitant volume to end-diastolic volume appears to help identify patients who may benefit from valve interventions. Secondary MR is not only attributed to geometric changes of the LV but also related to the structural changes in the mitral valve that include fibrosis of the mitral leaflets and changes in the extracellular matrix. The transition from mild to severe secondary MR can occur at different rates, from a slow LV remodeling process to a more abrupt process precipitated by an inciting event such as atrial fibrillation. Septal flash and apical rocking, two new visual markers of LV mechanical dyssynchrony, appear to be predictive of MR reduction following cardiac resynchronization therapy. Optimal guideline-directed medical therapy has been shown to decrease the severity of secondary MR effectively. A theoretical framework to characterize secondary MR as it relates to the onset of MR is proposed. Type A: Early onset of MR contemporaneous with myocardial injury. The maladaptive LV remodeling occurs in parallel with MR. Type B: LV remodeling proceeds without significant MR until the LV is moderately dilated, which coincides with or without inciting factors such as atrial fibrillation. Type C: LV remodeling proceeds after myocardial injury without significant MR until the LV is severely dilated. MR is a late manifestation of LV remodeling.

Severe stenosis of bioprosthetic valve due to late valve thrombosis.

The typical cause of bioprosthetic valve dysfunction over years is calcification of leaflets, pannus formation, or tears due to structural degeneration. Thrombosis is rare as the valves get endothelialized early on, and, hence, anticoagulation is not recommended beyond 6 months after valve replacement. While bioprosthetic valve thrombosis is unusual (0.03% to 0.34%/year), it can be associated with significant mortality and morbidity. Here, we present a case of a middle-aged man with history of bioprosthetic mitral valve who presented with syncopal episode and was referred to us for mitral valve replacement for tentative bioprosthetic valve degeneration and stenosis. However, preoperative work up revealed prosthetic valve thrombosis which was successfully treated with anticoagulation.

Revascularization in Cardiogenic Shock and Advanced Heart Failure.

PURPOSE OF REVIEW: Ischemic heart disease is the most common cause of heart failure with systolic dysfunction. The progressive course of heart failure characterized by increasing levels of care and worsening quality of life often indicates an advanced stage. Similarly, cardiogenic shock remains a major clinical problem with prohibitively high mortality rates despite major advances in clinical care. Here, we review the current treatment options and available data for revascularization in patients with ischemic cardiomyopathy, advanced heart failure, and cardiogenic shock. We also explore the emerging role of Interventional Heart Failure specialist within the Heart Team. RECENT FINDINGS: Although guideline-directed medical therapy remains the cornerstone treatment strategy for patients with advanced heart failure, coronary revascularization is sometimes indicated. There is a relatively paucity of evidence regarding different revascularization strategies and the use of acute mechanical circulatory support in patients with advanced heart failure and in those presenting with cardiogenic shock. A deep understating of the physiologic and hemodynamic effects of different acute mechanical support platforms is of paramount importance in preparation for revascularization in these patients. The decision regarding revascularization in patients with coronary artery disease in the setting of left ventricular dysfunction remains challenging. Clinical decision-making in these cases requires interdisciplinary discussion and assessment of the potential long-term survival derived from surgical revascularization against its higher perioperative risk.

Real life experience with bioresorbable-polymer everolimus-eluting stents. Is this an answer in search of a question?

Stent thrombosis and clinically driven restenosis are rare in the era of newer generation DES. The Synergy bioresorbable polymer DES appears to be comparable to other durable polymer and other bioabsorbable polymer DES in terms of safety and efficacy at 1-year post implantation. Further long-term study is needed to determine the specific role of the Synergy stent and other DES with bioabsorbable polymers.

Preclinical Alterations in Myocardial Microstructure in People with Metabolic Syndrome.

OBJECTIVE: Metabolic syndrome (MetS) can lead to myocardial fibrosis, diastolic dysfunction, and eventual heart failure. This study evaluated alterations in myocardial microstructure in people with MetS by using a novel algorithm to characterize ultrasonic signal intensity variation. METHODS: Among 254 participants without existing cardiovascular disease (mean age 42 ± 11 years, 75% women), there were 162 with MetS, 47 with obesity without MetS, and 45 nonobese controls. Standard echocardiography was performed, and a novel validated computational algorithm was used to investigate myocardial microstructure based on sonographic signal intensity and distribution. The signal intensity coefficient (SIC [left ventricular microstructure]) was examined. RESULTS: The SIC was significantly higher in people with MetS compared with people with (P < 0.001) and without obesity (P = 0.04), even after adjustment for age, sex, body mass index, hypertension, diabetes mellitus, and the ratio of triglyceride (TG) to high-density lipoprotein (HDL) cholesterol (P < 0.05 for all). Clinical correlates of SIC included TG concentrations (r = 0.21, P = 0.0007) and the TG/HDL ratio (r = 0.2, P = 0.001). CONCLUSIONS: This study's findings suggest that preclinical MetS and dyslipidemia in particular are associated with altered myocardial signal intensity variation. Future studies are needed to determine whether the SIC may help detect subclinical diseases in people with metabolic disease, with the ultimate goal of targeting preventive efforts.

Impaired right ventricular hemodynamics indicate preclinical pulmonary hypertension in patients with metabolic syndrome.

BACKGROUND: Metabolic disease can lead to intrinsic pulmonary hypertension in experimental models. The contributions of metabolic syndrome (MetS) and obesity to pulmonary hypertension and right ventricular dysfunction in humans remain unclear. We investigated the association of MetS and obesity with right ventricular structure and function in patients without cardiovascular disease. METHODS AND RESULTS: A total of 156 patients with MetS (mean age 44 years, 71% women, mean body mass index 40 kg/m(2)), 45 similarly obese persons without MetS, and 45 nonobese controls underwent echocardiography, including pulsed wave Doppler measurement of pulmonary artery acceleration time (PAAT) and ejection time. Pulmonary artery systolic pressure was estimated from PAAT using validated equations. MetS was associated with lower tricuspid valve e' (right ventricular diastolic function parameter), shorter PAAT, shorter ejection time, and larger pulmonary artery diameter compared with controls (P<0.05 for all). Estimated pulmonary artery systolic pressure based on PAAT was 42±12 mm Hg in participants with MetS compared with 32±9 and 32±10 mm Hg in obese and nonobese controls (P for ANOVA <0.0001). After adjustment for age, sex, hypertension, diabetes, body mass index, and triglycerides, MetS remained associated with a 20-ms-shorter PAAT (ß=-20.4, SE=6.5, P=0.002 versus obese). This association persisted after accounting for left ventricular structure and function and after exclusion of participants with obstructive sleep apnea. CONCLUSIONS: MetS is associated with abnormal right ventricular and pulmonary artery hemodynamics, as shown by shorter PAAT and subclinical right ventricular diastolic dysfunction. Estimated pulmonary artery systolic pressures are higher in MetS and preclinical metabolic heart disease and raise the possibility that pulmonary hypertension contributes to the pathophysiology of metabolic heart disease.