EG-MYH7 [R403E], EG-HFE [Cys282Tyr+/+], EV-HCMV, EG-A-TTR [V30M], EM-sarcoidosis SA-I, SA-II *The morphofunctional phenotype description (M) may contain more information using standard abbreviations, such as AVB, atrioventricular block; WPW, Wolff-Parkinson-White syndrome; LQT, prolongation of the QT interval; AF, atrial fibrillation; ↓R, low electrocardiogram voltages; ↓PR, short PR interval. † Organ (O) involvement in addition to the H subscript (for heart) should be expanded for the involvement of M, skeletal muscle; O, ocular system; A, auditory system; K, kidney; L, liver; N, nervous system; C, cutaneous; G, gastrointestinal system, and other comorbidities, including MR, mental retardation. ‡ Genetic (G) describes the available information about inheritance of the disease. It also provides complete information if the family history is not proven or unknown, and if genetic testing has not been performed or was negative for the mutation/mutations identified in the family. § The etiologic annotation (E) provides the facility for the synthetic description of the specific disease gene and mutation, as well as description of nongenetic etiology. || The functional annotation or staging (S) allows the addition of ACC/ AHA stage and NYHA functional class.

Objectives-Increased arterial wave reflection is a predictor of cardiovascular events and has been hypothesized to be a cofactor in the pathophysiology of heart failure. Whether increased wave reflection is inversely associated with left ventricular (LV) systolic function in subjects without heart failure is not clear.Methods-Arterial wave reflection and LV systolic function were assessed in 301 participants from the Cardiovascular Abnormalities and Brain Lesions (CABL) study using 2-dimensional echocardiography and applanation tonometry of the radial artery to derive central arterial waveform by a validated transfer function. Aortic augmentation index (AIx) and wasted energy index (WEi) were used as indices of wave reflection. LV systolic function was measured by ejection fraction (LVEF) and tissue Doppler imaging (TDI). Mitral annulus peak systolic velocity (Sm), peak longitudinal strain and strain rate were measured. Participants with history of coronary artery disease, atrial fibrillation, LVEF <50% or wall motion abnormalities were excluded.Results-Mean age of the study population was 68.3±10.2 years (64.1% women, 65% hypertensive). LV systolic function by TDI was lower with increasing wave reflection, whereas LVEF was not. In multivariate analysis, TDI parameters of LV longitudinal systolic function were significantly and inversely correlated to AIx and WEi (p values from 0.05 to 0.002).Conclusions-In a community cohort without heart failure and with normal LVEF, an increased arterial wave reflection was associated with subclinical reduction in LV systolic function assessed

The period following heart failure hospitalization (HFH) is a vulnerable time with high rates of death or recurrent HFH.OBJECTIVE To evaluate clinical characteristics, outcomes, and treatment response to vericiguat according to prespecified index event subgroups and time from index HFH in the Vericiguat Global Study in Subjects With Heart Failure With Reduced Ejection Fraction (VICTORIA) trial. DESIGN, SETTING, AND PARTICIPANTSAnalysis of an international, randomized, placebo-controlled trial. All VICTORIA patients had recent (<6 months) worsening HF (ejection fraction <45%). Index event subgroups were less than 3 months after HFH (n = 3378), 3 to 6 months after HFH (n = 871), and those requiring outpatient intravenous diuretic therapy only for worsening HF (without HFH) in the previous 3 months (n = 801). Data were analyzed between May 2, 2020, and May 9, 2020.INTERVENTION Vericiguat titrated to 10 mg daily vs placebo. MAIN OUTCOMES AND MEASURESThe primary outcome was time to a composite of HFH or cardiovascular death; secondary outcomes were time to HFH, cardiovascular death, a composite of all-cause mortality or HFH, all-cause death, and total HFH. RESULTS Among 5050 patients in the VICTORIA trial, mean age was 67 years, 24% were women, 64% were White, 22% were Asian, and 5% were Black. Baseline characteristics were balanced between treatment arms within each subgroup. Over a median follow-up of 10.8 months, the primary event rates were 40.9, 29.6, and 23.4 events per 100 patient-years in the HFH at less than 3 months, HFH 3 to 6 months, and outpatient worsening subgroups, respectively. Compared with the outpatient worsening subgroup, the multivariable-adjusted relative risk of the primary outcome was higher in HFH less than 3 months (adjusted hazard ratio, 1.48; 95% CI, 1.27-1.73), with a time-dependent gradient of risk demonstrating that patients closest to their index HFH had the highest risk. Vericiguat was associated with reduced risk of the primary outcome overall and in all subgroups, without evidence of treatment heterogeneity. Similar results were evident for all-cause death and HFH. Addtionally, a continuous association between time from HFH and vericiguat treatment showed a trend toward greater benefit with longer duration since HFH. Safety events (symptomatic hypotension and syncope) were infrequent in all subgroups, with no difference between treatment arms.CONCLUSIONS AND RELEVANCE Among patients with worsening chronic HF, those in closest proximity to their index HFH had the highest risk of cardiovascular death or HFH, irrespective of age or clinical risk factors. The benefit of vericiguat did not differ significantly across the spectrum of risk in worsening HF.

he Framingham offspring study has demonstrated that post-challenge hyperglycemia is an independent risk factor for cardiovascular disease, 1 and that stress hyperglycemia is one of the determinants of the outcome after myocardial infarction. 2,3 In this context, it is thought that coronary microvascular dysfunction related to stress hyperglycemia might be one of the possible reasons for the poor outcome in patients with acute myocardial infarction with stress hyperglycemia, and also for the improvement of epicardial coronary blood flow and outcome in these patients after nicorandil administration. 4 Thus, the association between acute hyperglycemia (AHG) and coronary microvascular function (ie, hyperemic response of coronary blood flow or coronary flow reserve) should be thoroughly examined. Although some studies have demonstrated that AHG may impair flow-mediated vasodilatation in the peripheral arteries, 5,6 which might be a predictor of future cardiovascular events, 7 the effect of AHG on coronary microvascular function has not been fully clarified. Increased oxidative stress 8 and/or sympathetic activation 9 have been demonstrated to contribute to impairment of coronary microvascular function, and both of these pathophysiological abnormalities are also observed during AHG.However, the influence of these abnormalities caused by AHG on coronary microvascular function has not been fully evaluated.Recently, transthoracic Doppler, which can be used to estimate coronary microvascular function in a non-invasive manner, has become feasible in the clinical setting. [10][11][12] Therefore, we chose to use it in the present study to evaluate the effects of AHG observed during the oral glucose tolerance test (OGTT) on coronary microvascular function, and the associations among changes in the hyperemic response of coronary blood flow velocity (CFV) or coronary flow velocity reserve (CFVR), oxidative stress, and increased sympathetic tone caused by AHG in subjects with atherosclerotic risk factors. Methods SubjectsTwenty-four patients receiving treatment for atherosclerotic risk factors (14 patients with hypertension, 6 with hypercholesterolemia, 3 with hypertension and hypercholesterolemia, and 1 patient with abnormal glucose intolerance) at Tokyo Medical University Hospital were enrolled in this study. None of the patients had any symptoms suggestive of coronary heart disease or changes on the electrocardiogram suggestive of myocardial ischemia. Furthermore, none of them showed any regional wall motion abnormality on echocardiography. Written informed consent was given by all the subjects prior to their participation and the study protocol was approved by the Ethics ComCirc J 2007; 71: 202 -206 (Received June 28, 2006; revised manuscript received September 12, 2006; accepted November 9, 2006) Background The effect of acute hyperglycemia (AHG) during the oral glucose tolerance test (OGTT) on coronary microvascular function was evaluated, as well as the associations among the changes in coronary microvascular functi...

BACKGROUND Although inflammatory markers may be associated with risk of cardiovascular events, few data are available regarding these markers and their association with left ventricular hypertrophy (LVH). We sought to evaluate whether inflammatory markers were independently associated with LVH in a multiethnic population in northern Manhattan. METHODS A population-based cross-sectional study was conducted in 660 participants without stroke, who had undergone both transthoracic echocardiography and testing for soluble tumor necrosis factor receptor (sTNFR) 1, interleukin (IL)-6, and high-sensitivity C-reactive protein (hsCRP). LV mass was calculated according to an established formula. LVH was defined as LV mass greater than the 90th percentile of the participants. RESULTS The mean age was 67.4 ± 8.8 years, 35.5% were men, 61.7% were Hispanic, 19.7% were black, and 18.6% were white. In univariate analyses, hsCRP, IL-6 and sTNFR1 were significantly associated with LV mass. Multiple linear regression analyses demonstrated that sTNFR1 (P = 0.0008) was associated with LV mass after adjusting for demographic and medical risk factors, but hsCRP and IL-6 were not. When all markers were included in the same model, sTNFR1 remained significant, but hsCRP and IL-6 did not. Compared with the lowest quartile of sTNFR1, those in the highest quartile were more likely to have LVH (Odds ratio = 1.84, 95% Confidence interval, 0.97 to 3.64, P = 0.06). CONCLUSIONS Soluble TNFR1, but not hsCRP nor IL-6, is independently associated with increased LV mass. Chronic subclinical inflammation including the TNFR1-associated system may contribute to LVH.