Prevalence and clinical associations of mitral and aortic regurgitation in patients with aortic stenosis.

BACKGROUND: Most guidelines directing clinicians to manage valve disease are directed at single valve lesions. Limited data exists to direct our understanding of how concomitant valve disease impacts the left ventricle (LV). METHODS: We identified 2817 patients with aortic stenosis (AS) from the echocardiography laboratory database between September 2012 and June 2018 who had a LV ejection fraction (EF) ≥50%. LV mass, LV mass index, LV systolic pressure (systolic blood pressure + peak aortic gradient). Covariates were collected from the electronic medical record. Multi-variate analysis of covariance was used to generate adjusted comparisons. RESULTS: Our population was 66% female, 17% African-American with a mean age of 65 years. Of note, 7.3% were noted to have significant (moderate/severe) aortic regurgitation (AR), and 11% had significant (moderate/severe) mitral regurgitation (MR). Adjusting for covariates at different levels, significant MR had a much stronger association with heart failure compared to those with significant AR (p < .001 vs. p = .313, respectively) at all levels of adjustment. Both significant mitral and AR exhibited an association with increasing left ventricular mass, even with adjustment for baseline demographics and clinical features (p < .001 vs. p = .007, respectively). CONCLUSION: In patients with AS, 16% also experience at least moderate MR or AR. Further, significant MR has a stronger association with heart failure than significant AR, even though both increase left ventricular mass. Those with moderate AS and significant MR or AR experience similar or higher levels of heart failure compared to severe AS without regurgitation. Mixed valve disease merits further studies to direct longitudinal management.

Newer Drugs to Reduce High Blood Pressure and Mitigate Hypertensive Target Organ Damage.

PURPOSE OF REVIEW: This review aims to investigate the blood pressure (BP)-lowering effects of emerging drugs developed to treat diabetic kidney disease and heart failure (HF). We summarize the potential pathophysiological mechanisms responsible for mitigating hypertensive target organ damage and evaluating the available clinical data on these newer drugs. RECENT FINDINGS: Nonsteroidal dihydropyridine-based mineralocorticoid receptor antagonists (MRAs), dual angiotensin II receptor-neprilysin inhibitors (valsartan with sacubitril), sodium-glucose cotransporter 2 inhibitors (SGLT2i), and soluble guanylate cyclase stimulators are new classes of chemical agents that have distinct mechanisms of action and have been shown to be effective for the treatment of cardiovascular (CV) disease (CVD), HF, and type 2 diabetes mellitus (T2D). These drugs can be used either alone or in combination with other antihypertensive and CV drugs. Among these, SGLT2i and valsartan with sacubitril offer new avenues to reduce CVD mortality. SGLT2i have a mild-to-moderate effect on BP lowering with a favorable effect on CV and renal hemodynamics and have been shown to produce a significant reduction in the incidence of major adverse CVD events (as monotherapy or add-on therapy) compared with controls (placebo or non-SGLT2i treatment). Most of the participants in these studies had hypertension (HTN) at baseline and were receiving antihypertensive therapy, including renin-angiotensin system blockers. The combination of valsartan with sacubitril also lowers BP in the short term and has demonstrated a striking reduction in CVD mortality and morbidity in HF patients with a reduced left ventricular ejection fraction. If widely adopted, these novel therapeutic agents hold significant promise for reducing the public health burden posed by HTN and CVD. Based on the results of several clinical trials and considering the high prevalence of HTN and T2D, these new classes of agents have emerged as powerful therapeutic tools in managing and lowering the BP of patients with diabetic kidney disease and HF.

Hypertension Across a Woman's Life Cycle.

PURPOSE OF REVIEW: We reviewed the effects of hypertension and the means to prevent and treat it across the spectrum of a woman's lifespan and identified gaps in sex-specific mechanisms contributing to hypertension in women that need to be addressed. RECENT FINDINGS: Hypertension continues to be an important public health problem for women across all life stages from adolescence through pregnancy, menopause, and older age. There remain racial, ethnic, and socioeconomic differences in hypertension rates not only overall but also between the sexes. Blood pressure cutoffs during pregnancy have not been updated to reflect the 2017 ACC/AHA changes due to a lack of data. Additionally, the mechanisms behind hypertension development in menopause, including sex hormones and genetic factors, are not well understood. In the setting of increasing inactivity and obesity, along with an aging population, hypertension rates are increasing in women. Screening and management of hypertension throughout a women's lifespan are necessary to reduce the burden of cardiovascular disease, and further research to understand sex-specific hypertension mechanisms is needed.

Optimizing The Management of Obese HFpEF Phenotype: Can We Mind Both The Heart and The Kidney?

The adverse prognostic implications of significant renal dysfunction during treatment of acute decompensated heart failure (HF) in patients with obese HF and preserved ejection fraction (HFpEF) provide strong rationale for development of therapeutic strategies that enhance decongestion while preserving renal function in this cohort. The combination of preload sensitivity, intrinsic renal dysfunction related to obesity, glomerular hyperfiltration, reversible renal hypoperfusion (poor renal arterial perfusion and renal venous congestion), and decreased systemic vascular resistance in obesity may predispose patients to renal hemodynamic compromise during diuresis. Thus, serum creatinine increase should not be evaluated in isolation but rather considered in the context of the entire clinical picture in patients with obese HFpEF.

Obstructive coronary artery disease with a coronary artery calcium score of 0: A case report.

Coronary artery calcium (CAC) scoring has emerged as a useful tool in identifying patients who may benefit from more aggressive risk factor modification and for prognostication. Although a CAC score of 0 is associated with a very low prevalence of obstructive epicardial coronary artery disease and low event rates, it can also provide a false sense of reassurance. We present a case of a 39-year-old woman with a CAC score of 0 obtained as part of a coronary computerized tomography angiography study that was ultimately found to have significant left anterior descending artery disease requiring percutaneous coronary intervention and a stent.

Prediabetes and the association with unrecognized myocardial infarction in the multi-ethnic study of atherosclerosis.

BACKGROUND: With one-quarter of initial myocardial infarctions (MI) being unrecognized MI (UMI), recognition is critical to minimize further cardiovascular risk. Diabetes mellitus is an established risk factor for UMI. If impaired fasting glucose (IFG) also increased the risk for UMI, it would represent a significant public health challenge due to the rapid worldwide increase in IFG prevalence. We compared participants with IFG to those with normal fasting glucose (NFG) to determine if IFG was associated with UMIs. METHODS: We performed cross-sectional analyses from the MESA, a population-based cohort study. There were 6,814 participants recruited during July 2000 to September 2002 from the general community at 6 field sites. After excluding those with diabetes mellitus or missing variables, 5,885 participants were included. At baseline, there were 4,955 participants with NFG and 930 participants with IFG. The main outcome was an UMI defined by the presence of pathological Q waves or minor Q waves with ST-T abnormalities on initial 12-lead electrocardiogram. Logistic regression was used to generate crude ORs and adjust for covariates. RESULTS: There was a higher prevalence of UMI in those with IFG compared with those with NFG [3.5% (n = 72) vs 1.4% (n = 30)]. After adjustment for multiple risk factors, there was a higher odds of an UMI among those with IFG compared with those with NFG [OR: 1.60 (95% CI: 1.0-2.5); P = .048]. CONCLUSIONS: Impaired fasting glucose is associated with unrecognized myocardial infarctions in a multi-ethnic population free of baseline cardiovascular disease.

Right ventricular stress-induced perfusion defects and late gadolinium enhancement in coronary artery disease.

OBJECTIVE: The assessment of right ventricular (RV) perfusion defects has remained challenging during vasodilator stress perfusion with cardiovascular magnetic resonance (CMR). The significance of RV signal abnormalities during vasodilator stress perfusion and late gadolinium-enhanced CMR is yet uncertain. METHODS: Among 61 individuals who underwent adenosine CMR stress testing before cardiac catheterization, we assessed the severity of coronary artery stenoses, mortality, the presence of stress and rest perfusion defects, as well as the presence of late gadolinium enhancement (LGE). RESULTS: Right ventricular stress-induced perfusion defects were positively associated with left anterior descending artery and proximal right coronary artery stenoses but were negatively associated with left circumflex artery stenoses. The presence of RVLGE was associated with mortality, but 77% of those with RVLGE also had left ventricular LGE. CONCLUSIONS: Proximal right coronary artery and left anterior descending artery stenoses are positively associated, whereas left circumflex artery stenoses are negatively associated with RV stress-induced perfusion defects. Right ventricular LGE was associated with mortality, but further study is needed to determine whether this is independent of left ventricular LGE.

Echocardiography-derived tricuspid regurgitant jet velocity is an important marker for the progression of sickle-cell disease.

BACKGROUND: Although echocardiography-derived tricuspid regurgitant jet velocity (TRV) is associated with increased mortality in sickle-cell disease (SCD), it is unclear whether increased TRV is a marker of multiorgan disease due to systemic vasculopathy or related to increased pulmonary artery systolic pressure with episodes of multiple acute chest syndrome (ACS). METHODS: Our study analyzed 148 consecutive patients with transthoracic echocardiography with TRV data, who came to our adult SCD Clinic at the Wake Forest Baptist Medical Center. For our analysis, we took TRV ≥ 2.5 m/s as elevated. Patients were followed on average for 9 years. RESULTS: TRV ≥ 3 m/s was significantly associated with increased mortality (p < 0.001), thromboembolism (p < 0.001), hospitalization for ACS (p < 0.001), supraventricular arrhythmia (p = 0.028), right ventricular (RV) dilation, decreased hemoglobin and increased creatinine. Patients with a progressive increase in TRV during follow-up had increased mortality (36.7 vs. 8.6%, p = 0.007) and increased ACS (45 vs. 5.7%, p < 0.001). Death was independently associated with TRV ≥ 3 m/s (p = 0.023), ACS (p = 0.001) and increased RV basal diameter (p = 0.003). CONCLUSIONS: TRV is an important global marker for the severity and progression of SCD, and carries a significant prognostic implication.

Abnormal Fasting Glucose Increases Risk of Unrecognized Myocardial Infarctions in an Elderly Cohort.

OBJECTIVES: To investigate glucose levels as a risk factor for unrecognized myocardial infarctions (UMIs). DESIGN: Cohort SETTING: Cardiovascular Health Study. PARTICIPANTS: Individuals aged 65 and older with fasting glucose measurements (N=4,355; normal fasting glucose (NFG), n = 2,041; impaired fasting glucose (IFG), n = 1,706; DM: n = 608; 40% male, 84% white, mean age 72.4 ± 5.6). MEASUREMENTS: The relationship between glucose levels and UMI was examined. Participants with prior coronary heart disease (CHD) or UMI on initial electrocardiography were excluded. Using Minnesota codes, UMI was identified according to the presence of pathological Q-waves or minor Q-waves with ST-T abnormalities. Crude and adjusted hazard ratios (HRs) were calculated. Analyses were adjusted for age, sex, body mass index (BMI), hypertension, antihypertensive and lipid-lowering medication use, total cholesterol, high-density lipoprotein cholesterol, and smoking status. RESULTS: Over a mean follow-up of 6 years, there were 459 incident UMIs (NFG, n=202; IFG, n=183; DM, n=74). Participants with IFG were slightly more likely than those with NFG to experience a UMI (hazard ratio (HR)=1.11, 95% confidence interval (CI)=0.91-1.36, p = .30), and those with DM were more likely than those with NFG to experience a UMI (HR=1.65, 95% CI=1.25-2.13, p < .001). After adjustment HR for UMI in IFG those with IFG were no more likely than those with NFG to experience a UMI (HR=1.01, 95% CI=0.82-1.24, p = .93), whereas those with DM were more likely than those with NFG to experience a UMI (HR=1.37, 95% CI=1.02-1.81, p = .03). The 2-hour oral glucose tolerance test was not statistically significantly associated with UMI. CONCLUSION: Fasting glucose status, particularly in the diabetic range, forecasted UMI during 6 years of follow-up in elderly adults. Further studies are needed to clarify the level of glucose at which risk is greater. J Am Geriatr Soc 67:43-49, 2019.

Improvement in systolic function in left ventricular non-compaction cardiomyopathy: A case report.

This is a case of a 48-year-old man who presented with a pulmonary embolism and was found to have left ventricular non-compaction cardiomyopathy. Initial echocardiograms demonstrated prominent apical trabeculations with reduced biventricular function. These findings were further confirmed and characterized by cardiac magnetic resonance imaging. He met all major criteria used to identify left ventricular non-compaction cardiomyopathy. He underwent medical management for heart failure and during follow-up was noted to have significant improvement in left ventricular systolic function and symptoms. While most management attention is focused on rhythm disturbances or embolic risk, particular attention should also be exercised to ensure that heart failure medical therapy is optimized. While many with left ventricular non-compaction cardiomyopathy have irreversible dysfunction, this case highlights that there may be some who will respond well to aggressive medical therapy. The diagnosis and medical management of left ventricular non-compaction cardiomyopathy are reviewed in light of our patient and his clinical course. .

Right ventricular morphology and systolic function in left ventricular noncompaction cardiomyopathy.

The distinction between normal right ventricular (RV) trabeculations from abnormal has been difficult. We evaluated whether RV volume and function are related to left ventricular (LV) noncompaction (NC) cardiomyopathy and clinical events. Trabeculations or possible LVNC by cardiac magnetic resonance imaging was retrospectively observed among 105 consecutive cases. We measured LV end-systolic (ES) noncompacted-to-compacted ratio, RV ejection fraction (EF), RV apical trabecular thickness, and RV end-diastolic (ED) noncompacted-to-compacted ratio. A control group of 40 subjects was also reviewed to assess the exploratory measures. Comparing those with LVES noncompacted-to-compacted ratio ≥2, those with LVES noncompacted-to-compacted ratio <2, and the normal control group, adjusted means for RV apical trabecular thickness and RVED noncompacted-to-compacted ratio were generated. Logistic regression was used to evaluate the association of composite events traditionally associated with LVNC with RVEF after adjustment for aforementioned covariates, cardiovascular risk factors, delayed enhancement, LVEF, and LVES noncompacted-to-compacted ratio. Analysis of RV morphology found greater apical trabecular thickness among those with LVES noncompacted-to-compacted ratio ≥2 compared with those with LVES noncompacted-to-compacted ratio <2 or normal control group (31 ± 5 vs 27 ± 2.6 vs 22 ± 4 mm; p = 0.03 and p = 0.003, respectively). There was no difference between the groups in relation to the RVED noncompacted-to-compacted ratio. Low RVEF and LVES noncompacted-to-compacted ratio ≥2 had significant association with clinical events in this population even after adjusting for clinical and imaging parameters (p = 0.04 and p <0.001, respectively). In conclusion, RV dysfunction in a morphologic LVNC population is strongly associated with adverse clinical events. LVNC is associated with increased trabeculations of the RV apex.