Aims Almost half of African American (AA) men and women have cardiovascular disease (CVD). Detection of prevalent CVD in community settings would facilitate secondary prevention of CVD. We sought to develop a tool for automated CVD detection. Methods and Results Participants from the Jackson Heart Study (JHS) with analyzable ECGs (n = 3,679; age, 62±12 years; 36% men) were included. Vectorcardiographic (VCG) metrics QRS, T, and spatial ventricular gradient (SVG) vectors’ magnitude and direction, and traditional ECG metrics were measured on 12-lead ECG. Random forests, convolutional neural network (CNN), lasso, adaptive lasso, plugin lasso, elastic net, ridge, and logistic regression models were developed in 80% and validated in 20% samples. We compared models with demographic, clinical, and VCG input (43 predictors) and those after the addition of ECG metrics (695 predictors). Prevalent CVD was diagnosed in 411 out of 3,679 participants (11.2%). Machine-learning models detected CVD with ROC AUC 0.69-0.74. There was no difference in CVD detection accuracy between models with VCG and VCG+ECG input. Models with VCG input were better calibrated than models with ECG input. Plugin-based lasso model consisting of only two predictors (age and peak QRS-T angle) detected CVD with AUC 0.687 (95%CI 0.625-0.749), which was similar (P = 0.394) to the CNN (0.660; 95%CI 0.597-0.722) and better (P < 0.0001) than random forests (0.512; 95% CI 0.493-0.530). Conclusions Simple model (age and QRS-T angle) can be used for prevalent CVD detection in limited-resources community settings, which opens an avenue for secondary prevention of CVD in underserved communities.
The arrhythmogenic potential of diuretic-induced hypokalemia in patients with uncomplicated hypertension has been controversial. Thirty-two hypertensive patients with previous diuretic-induced hypokalemia, normal 24-hour ambulatory ECG monitoring, and normal exercise testing were treated with 100 mg hydrochlorothiazide (HCTZ) daily (Group 1) to induce hypokalemia or with a combination of HCTZ with amiloride (Group 2) to attempt to maintain plasma potassium levels in the normal range during diuretic therapy. Those Group 1 patients (Group 1A) with increased ventricular ectopic activity (VEA) during HCTZ therapy were subsequently potassium-repleted with amiloride and with supplemental potassium chloride to evaluate the effect of these treatments on VEA. One Group 1 patient died suddenly after 12 days of HCTZ therapy. Autopsy findings suggested an arrhythmic death. Six Group 1 patients who had increased VEA with HCTZ treatment had reductions in VEA with amiloride or supplemental potassium chloride. Group 2 patients did not have a significant increase in VEA. Thus, diuretic therapy appears to cause VEA primarily by electrolyte changes that are induced.
Summary Background Left ventricular false tendons (LVFTs) are chord-like structures that traverse the LV cavity and are generally considered to be benign. However, they have been associated with arrhythmias, LV hypertrophy and LV dilation in some small studies. Hypothesis LVFTs are associated with LV structural and functional changes assessed by echocardiography. Methods We retrospectively evaluated echocardiographic and clinical parameters of 126 patients identified as having LVFTs within the past 2 years and compared them to 85 age-matched controls without LVFTs. Results There were no significant differences in age (52±18 vs 54±18 years, p=0.37), sex (55 vs 59 % men, p=0.49), race (36 vs 23% white, p=0.07), systolic blood pressure (SBP, 131±22 vs 132±23 mmHg, p=0.76) or body mass index (BMI, 31±8 vs 29±10 kg/m2, p=0.07) between controls and patients with LVFTs, respectively. Patients with LVFTs had more prevalent heart failure (43% vs 21%, p=0.001). Patients with LVFTs had more LV dilation, were 2.5 times more likely to have moderate to severe mitral regurgitation, had more severe diastolic dysfunction and reduced LV systolic function (18% lower) compared with controls (all p<0.05). After adjustment for covariates, basal and middle LVFT locations were associated with reduced LV systolic function (p <0.01) and middle LVFTs were associated with LV dilation (p<0.01). Conclusions Our findings suggest LVFTs may not be benign variants and basal and middle LVFTs may have more deleterious effects. Further prospective studies should be performed to determine their pathophysiological significance and if they play a causal role in LV dysfunction.
High-level synthesis (HLS), which refers to the automatic compilation of software into hardware, is rapidly gaining popularity. In a world increasingly reliant on application-specific hardware accelerators, HLS promises hardware designs of comparable performance and energy efficiency to those coded by hand in a hardware description language such as Verilog, while maintaining the convenience and the rich ecosystem of software development. However, current HLS tools cannot always guarantee that the hardware designs they produce are equivalent to the software they were given, thus undermining any reasoning conducted at the software level. Furthermore, there is mounting evidence that existing HLS tools are quite unreliable, sometimes generating wrong hardware or crashing when given valid inputs. To address this problem, we present the first HLS tool that is mechanically verified to preserve the behaviour of its input software. Our tool, called Vericert, extends the CompCert verified C compiler with a new hardware-oriented intermediate language and a Verilog back end, and has been proven correct in Coq. Vericert supports most C constructs, including all integer operations, function calls, local arrays, structs, unions, and general control-flow statements. An evaluation on the PolyBench/C benchmark suite indicates that Vericert generates hardware that is around an order of magnitude slower (only around 2× slower in the absence of division) and about the same size as hardware generated by an existing, optimising (but unverified) HLS tool.
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