Lankenau Heart Institute

BACKGROUND: Optical sensors on wearable devices can detect irregular pulses. The ability of a smartwatch application (app) to identify atrial fibrillation during typical use is unknown. METHODS: Participants without atrial fibrillation (as reported by the participants themselves) used a smartphone (Apple iPhone) app to consent to monitoring. If a smartwatch-based irregular pulse notification algorithm identified possible atrial fibrillation, a telemedicine visit was initiated and an electrocardiography (ECG) patch was mailed to the participant, to be worn for up to 7 days. Surveys were administered 90 days after notification of the irregular pulse and at the end of the study. The main objectives were to estimate the proportion of notified participants with atrial fibrillation shown on an ECG patch and the positive predictive value of irregular pulse intervals with a targeted confidence interval width of 0.10. RESULTS: We recruited 419,297 participants over 8 months. Over a median of 117 days of monitoring, 2161 participants (0.52%) received notifications of irregular pulse. Among the 450 participants who returned ECG patches containing data that could be analyzed - which had been applied, on average, 13 days after notification - atrial fibrillation was present in 34% (97.5% confidence interval [CI], 29 to 39) overall and in 35% (97.5% CI, 27 to 43) of participants 65 years of age or older. Among participants who were notified of an irregular pulse, the positive predictive value was 0.84 (95% CI, 0.76 to 0.92) for observing atrial fibrillation on the ECG simultaneously with a subsequent irregular pulse notification and 0.71 (97.5% CI, 0.69 to 0.74) for observing atrial fibrillation on the ECG simultaneously with a subsequent irregular tachogram. Of 1376 notified participants who returned a 90-day survey, 57% contacted health care providers outside the study. There were no reports of serious app-related adverse events. CONCLUSIONS: The probability of receiving an irregular pulse notification was low. Among participants who received notification of an irregular pulse, 34% had atrial fibrillation on subsequent ECG patch readings and 84% of notifications were concordant with atrial fibrillation. This siteless (no on-site visits were required for the participants), pragmatic study design provides a foundation for large-scale pragmatic studies in which outcomes or adherence can be reliably assessed with user-owned devices. (Funded by Apple; Apple Heart Study ClinicalTrials.gov number, NCT03335800.).

BACKGROUND: Smartwatch and fitness band wearable consumer electronics can passively measure pulse rate from the wrist using photoplethysmography (PPG). Identification of pulse irregularity or variability from these data has the potential to identify atrial fibrillation or atrial flutter (AF, collectively). The rapidly expanding consumer base of these devices allows for detection of undiagnosed AF at scale. METHODS: The Apple Heart Study is a prospective, single arm pragmatic study that has enrolled 419,093 participants (NCT03335800). The primary objective is to measure the proportion of participants with an irregular pulse detected by the Apple Watch (Apple Inc, Cupertino, CA) with AF on subsequent ambulatory ECG patch monitoring. The secondary objectives are to: 1) characterize the concordance of pulse irregularity notification episodes from the Apple Watch with simultaneously recorded ambulatory ECGs; 2) estimate the rate of initial contact with a health care provider within 3 months after notification of pulse irregularity. The study is conducted virtually, with screening, consent and data collection performed electronically from within an accompanying smartphone app. Study visits are performed by telehealth study physicians via video chat through the app, and ambulatory ECG patches are mailed to the participants. CONCLUSIONS: The results of this trial will provide initial evidence for the ability of a smartwatch algorithm to identify pulse irregularity and variability which may reflect previously unknown AF. The Apple Heart Study will help provide a foundation for how wearable technology can inform the clinical approach to AF identification and screening.

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OBJECTIVES: This study sought to characterize the electrocardiographic patterns predictive of left ventricular sites of origin of repetitive monomorphic ventricular tachycardia (RMVT). BACKGROUND: RMVT typically arises from the right ventricular outflow tract (RVOT) in patients without structural heart disease. The incidence of left ventricular sites of origin in this syndrome is unknown. METHODS: Detailed endocardial mapping of the RVOT was performed in 33 consecutive patients with RMVT during attempted radiofrequency ablation. Left ventricular mapping was also performed if pace maps obtained from the RVOT did not reproduce the configuration of the induced tachycardia. RESULTS: Pace maps identical in configuration to the induced tachycardia were obtained from the RVOT in 29 of 33 patients. Application of radiofrequency energy at sites guided by pace mapping resulted in elimination of RMVT in 24 (83%) of 29 patients. In four patients (12%), pace maps obtained from the RVOT did not match the induced tachycardia. All four patients had a QRS configuration during RMVT with precordial R wave transitions at or before lead V2. In two patients, RMVT was mapped to the mediosuperior aspect of the mitral valve annulus, near the left fibrous trigone; catheter ablation at that site was successful in both. In two patients, RMVT was mapped to the basal aspect of the superior left ventricular septum. Catheter ablation was not attempted because His bundle deflections were recorded from this site during sinus rhythm. CONCLUSIONS: RMVT can arise from the outflow tract of both the right and left ventricles. RMVTs with a precordial R wave transition at or before lead V2 are consistent with a left ventricular origin.

Aim: The primary objective was to compare apixaban to heparin/vitamin K antagonist (VKA) in patients with atrial fibrillation (AF) and ≤48 h anticoagulation prior to randomization undergoing cardioversion. Methods: One thousand five hundred patients were randomized. The apixaban dose of 5 mg b.i.d. was reduced to 2.5 mg b.i.d. in patients with two of the following: age ≥ 80 years, weight ≤ 60 kg, or serum creatinine ≥ 133 µmol/L. To expedite cardioversion, at the discretion of the investigator, imaging and/or a loading dose of 10 mg (down-titrated to 5 mg) was allowed. The endpoints for efficacy were stroke, systemic embolism (SE), and death. The endpoints for safety were major bleeding and clinically relevant non-major (CRNM) bleeding. Results: There were 1038 active and 300 spontaneous cardioversions; 162 patients were not cardioverted. Imaging was performed in 855 patients, and 342 received a loading dose of apixaban. Comparing apixaban to heparin/VKA in the full analysis set, there were 0/753 vs. 6/747 strokes [relative risk (RR) 0; 95% confidence interval (95% CI) 0-0.64; nominal P = 0.015], no SE, and 2 vs. 1 deaths (RR 1.98; 95% CI 0.19-54.00; nominal P > 0.999). In the safety population, there were 3/735 vs. 6/721 major (RR 0.49; 95% CI 0.10-2.07; nominal P = 0.338) and 11 vs. 13 CRNM bleeding events (RR 0.83; 95% CI 0.34-1.89; nominal P = 0.685). On imaging, 60/61 with thrombi continued randomized treatment; all (61) were without outcome events. Conclusions: Rates of strokes, systemic emboli, deaths, and bleeds were low for both apixaban and heparin/VKA treated AF patients undergoing cardioversion. Clinical Trials.gov number: NCT02100228.

BACKGROUND: Randomized data comparing outcomes of transcatheter aortic valve replacement (TAVR) with surgery in low-surgical risk patients at time points beyond 2 years is limited. This presents an unknown for physicians striving to educate patients as part of a shared decision-making process. OBJECTIVES: The authors evaluated 3-year clinical and echocardiographic outcomes from the Evolut Low Risk trial. METHODS: Low-risk patients were randomized to TAVR with a self-expanding, supra-annular valve or surgery. The primary endpoint of all-cause mortality or disabling stroke and several secondary endpoints were assessed at 3 years. RESULTS: There were 1,414 attempted implantations (730 TAVR; 684 surgery). Patients had a mean age of 74 years and 35% were women. At 3 years, the primary endpoint occurred in 7.4% of TAVR patients and 10.4% of surgery patients (HR: 0.70; 95% CI: 0.49-1.00; P = 0.051). The difference between treatment arms for all-cause mortality or disabling stroke remained broadly consistent over time: -1.8% at year 1; -2.0% at year 2; and -2.9% at year 3. The incidence of mild paravalvular regurgitation (20.3% TAVR vs 2.5% surgery) and pacemaker placement (23.2% TAVR vs 9.1% surgery; P < 0.001) were lower in the surgery group. Rates of moderate or greater paravalvular regurgitation for both groups were <1% and not significantly different. Patients who underwent TAVR had significantly improved valve hemodynamics (mean gradient 9.1 mm Hg TAVR vs 12.1 mm Hg surgery; P < 0.001) at 3 years. CONCLUSIONS: Within the Evolut Low Risk study, TAVR at 3 years showed durable benefits compared with surgery with respect to all-cause mortality or disabling stroke. (Medtronic Evolut Transcatheter Aortic Valve Replacement in Low Risk Patients; NCT02701283).

Pace mapping used to locate the site for ablation of idiopathic right ventricular outflow tract (RVOT) ventricular tachycardia remains difficult and time-consuming. A method to facilitate pace mapping and the most common site of ablation of this tachycardia are reported. In 18 consecutive patients with RVOT ventricular tachycardia, electrocardiographic criteria based on the QRS orientation in lead 1 and the R wave progression in the precordial leads were used to find pace maps matching the arrhythmia. Identical pace maps were obtained on the septum of the RVOT in 16 patients and resulted in successful ablations. These sites were concentrated in the anterior superior aspect of the RVOT determined by fluoroscopic imaging. In the remaining two cases identical pace maps could not be found in this area. The results of this study narrow the anatomic location for radiofrequency ablation of idiopathic RVOT ventricular tachycardia. This is the first description of an electrocardiography-guided approach to finding an identical pace map in the RVOT.

OBJECTIVES: We report the comprehensive results of the first consecutive 3,000 patients treated in an excimer laser coronary angioplasty registry. BACKGROUND: Excimer laser coronary angioplasty involves the use of a pulsed, 308-nm ultraviolet laser transmitted by optical fibers to reduce coronary stenoses. Preliminary reports have described safety and efficacy profiles in small numbers of patients. METHODS: Patients were enrolled in a prospective, nonrandomized manner. The catheters used were 1.3, 1.6, 2.0, 2.2 and 2.4 mm in diameter, at energy densities up to 70 mJ/mm2. Procedures were performed by standard angioplasty technique with conventional guide catheters. RESULTS: Seventy-five percent of patients were male, 68% were in Canadian Cardiovascular Society functional class III or IV and the cohort included 3,592 lesions. Procedural success (final stenosis < or = 50% without in-hospital Q wave myocardial infarction, coronary artery bypass surgery or death) was 90% and did not differ between the first 2,000 and the last 1,000 patients treated. There was no significant difference in success or complication rates with respect to lesion length, nor were there differences between selected complex and simple lesions. Complications included in-hospital bypass surgery (3.8%), Q wave myocardial infarction (2.1%) and death (0.5%). Coronary artery perforation occurred in 1.2% of patients (1% of lesions) but significantly decreased to 0.4% in the last 1,000 patients (0.3% of lesions). Angiographic dissection occurred in 13% of lesions, transient occlusion in 3.4% and sustained occlusion in 3.1%. Comprehensive lesion morphologic data collected in the latter portion of the study showed the procedure predominantly limited to American College of Cardiology-American Heart Association type B2 and C lesions, with no significant difference in short-term outcome between groups. CONCLUSIONS: Excimer laser angioplasty can be safely and effectively applied, even in a variety of complex lesions not well suited for percutaneous transluminal coronary angioplasty. These types may include aorto-ostial, long lesions, total occlusions crossable with a wire, diffuse disease and vein grafts. Most recent data show a trend for the selection of predominantly complex lesions and a reduction in the incidence of perforation. This procedure may broaden the therapeutic window for the interventional treatment of selected complex coronary artery disease.

The primary goal of this investigation was to describe the effect of terfenadine on the QT interval corrected for heart rate (QTc) of the scalar electrocardiogram (ECG). The design was double-blind, four-period crossover, dose escalation, which involved 28 normal healthy volunteers and 28 patients with stable cardiovascular disease. At baseline, the normal subjects had a mean QTc interval of 407 msec, whereas the patients with cardiovascular disease had a mean QTc interval of 417 msec (p<0.01). The largest increase in mean QTc on terfenadine was 24 msec in a normal subject and 28 msec in a patient with cardiovascular disease. The longest average QTc observed was 449 msec and 501 msec in any normal subject and patient with cardiovascular disease, respectively. Compared to baseline, terfenadine 60 mg twice daily is associated with a QTc increase of 6 msec in normal subjects and a 12 msec increase in patients with cardiovascular disease (p<0.01 vs baseline; p>0.05 when the two populations were compared). Although the QTc increase from baseline are statistically significant, the magnitude of the spontaneous variability in QTc in the same patients is much greater. Because 40 ECGs were obtained while taking placebo in each participant, the spontaneous variability in QTc interval with placebo was also described. Only one of the 28 normal subjects had a mean baseline QTc=440 msec, yet 14 of the 28 normal subjects had at lease one of the 40 placebo ECGs with a QTc=440 msec. The 28 patients with cardiovascular disease had a mean QTc at baseline of 417 msec; yet 20 of 28 had at lease one ECG on placebo with a QTc interval = 440 msec. On the average, the QTc fluctuated 56 msec in each patient during placebo administration. From the observed placebo variability, we calculated that an increase in QTc of=35 msec while receiving drug therapy is likely to represent a drug effect at the 95% confidence interval.

Background: Long QT syndrome (LQTS) is a rare genetic disorder and a major preventable cause of sudden cardiac death in the young. A causal rare genetic variant with large effect size is identified in up to 80% of probands (genotype positive) and cascade family screening shows incomplete penetrance of genetic variants. Furthermore, a proportion of cases meeting diagnostic criteria for LQTS remain genetically elusive despite genetic testing of established genes (genotype negative). These observations raise the possibility that common genetic variants with small effect size contribute to the clinical picture of LQTS. This study aimed to characterize and quantify the contribution of common genetic variation to LQTS disease susceptibility. Methods: We conducted genome-wide association studies followed by transethnic meta-analysis in 1656 unrelated patients with LQTS of European or Japanese ancestry and 9890 controls to identify susceptibility single nucleotide polymorphisms. We estimated the common variant heritability of LQTS and tested the genetic correlation between LQTS susceptibility and other cardiac traits. Furthermore, we tested the aggregate effect of the 68 single nucleotide polymorphisms previously associated with the QT-interval in the general population using a polygenic risk score. Results: Genome-wide association analysis identified 3 loci associated with LQTS at genome-wide statistical significance ( P &lt;5×10 −8 ) near NOS1AP , KCNQ1 , and KLF12 , and 1 missense variant in KCNE1 (p.Asp85Asn) at the suggestive threshold ( P &lt;10 −6 ). Heritability analyses showed that ≈15% of variance in overall LQTS susceptibility was attributable to common genetic variation ( h2SNP 0.148; standard error 0.019). LQTS susceptibility showed a strong genome-wide genetic correlation with the QT-interval in the general population (r g =0.40; P =3.2×10 −3 ). The polygenic risk score comprising common variants previously associated with the QT-interval in the general population was greater in LQTS cases compared with controls ( P &lt;10−13), and it is notable that, among patients with LQTS, this polygenic risk score was greater in patients who were genotype negative compared with those who were genotype positive ( P &lt;0.005). Conclusions: This work establishes an important role for common genetic variation in susceptibility to LQTS. We demonstrate overlap between genetic control of the QT-interval in the general population and genetic factors contributing to LQTS susceptibility. Using polygenic risk score analyses aggregating common genetic variants that modulate the QT-interval in the general population, we provide evidence for a polygenic architecture in genotype negative LQTS.

OBJECTIVES: This study sought to investigate the role of secretory phospholipase A2 (sPLA2)-IIA in cardiovascular disease. BACKGROUND: Higher circulating levels of sPLA2-IIA mass or sPLA2 enzyme activity have been associated with increased risk of cardiovascular events. However, it is not clear if this association is causal. A recent phase III clinical trial of an sPLA2 inhibitor (varespladib) was stopped prematurely for lack of efficacy. METHODS: We conducted a Mendelian randomization meta-analysis of 19 general population studies (8,021 incident, 7,513 prevalent major vascular events [MVE] in 74,683 individuals) and 10 acute coronary syndrome (ACS) cohorts (2,520 recurrent MVE in 18,355 individuals) using rs11573156, a variant in PLA2G2A encoding the sPLA2-IIA isoenzyme, as an instrumental variable. RESULTS: PLA2G2A rs11573156 C allele associated with lower circulating sPLA2-IIA mass (38% to 44%) and sPLA2 enzyme activity (3% to 23%) per C allele. The odds ratio (OR) for MVE per rs11573156 C allele was 1.02 (95% confidence interval [CI]: 0.98 to 1.06) in general populations and 0.96 (95% CI: 0.90 to 1.03) in ACS cohorts. In the general population studies, the OR derived from the genetic instrumental variable analysis for MVE for a 1-log unit lower sPLA2-IIA mass was 1.04 (95% CI: 0.96 to 1.13), and differed from the non-genetic observational estimate (OR: 0.69; 95% CI: 0.61 to 0.79). In the ACS cohorts, both the genetic instrumental variable and observational ORs showed a null association with MVE. Instrumental variable analysis failed to show associations between sPLA2 enzyme activity and MVE. CONCLUSIONS: Reducing sPLA2-IIA mass is unlikely to be a useful therapeutic goal for preventing cardiovascular events.

Purpose: To evaluate the performance of peripheral intravascular lithotripsy (IVL) in a real-world setting during endovascular treatment of multilevel calcified peripheral artery disease (PAD). Materials and Methods: The Disrupt PAD III Observational Study ( ClinicalTrials.gov identifier NCT02923193) is a prospective, nonrandomized, multicenter, single-arm observational study assessing the acute safety and effectiveness of the Shockwave Peripheral IVL System for the treatment of calcified, stenotic lower limb arteries. Patients were eligible if they had claudication or chronic limb-threatening ischemia and moderate or severe arterial calcification. Between November 2017 and August 2018, 200 patients (mean age 72.5±8.7 years; 148 men) were enrolled across 18 sites and followed through hospital discharge. Results: In the 220 target lesions, IVL was more commonly used in combination with other balloon-based technologies (53.8%) and less often with concomitant atherectomy or stenting (19.8% and 29.9%, respectively). There was a 3.4-mm average acute gain at the end of procedure; the final mean residual stenosis was 23.6%. Angiographic complications were rare, with only 2 type D dissections and a single perforation following drug-coated balloon inflation (unrelated to the IVL procedure). There was no abrupt closure, distal embolization, no reflow, or thrombotic event. Conclusion: Use of peripheral IVL to treat severely calcified, stenotic PAD in a real-world study demonstrated low residual stenosis, high acute gain, and a low rate of complications despite the complexity of disease.

ObjectiveTo evaluate the midterm hemodynamic performance and clinical outcomes of the Trifecta aortic pericardial valve.MethodsIn a multicenter, prospective, nonrandomized, follow-up study, 710 patients underwent surgical implantation of a pericardial stented aortic prosthesis (Trifecta valve; St Jude Medical, St. Paul, Minn). The valve is constructed from bovine pericardium mounted externally onto a titanium stent. Subjects were followed on an annual basis over 6 years.ResultsOperations were performed from 2007 to 2009, and mean age was 72.4 ± 9.3 years; 471 of 710 (66.3%) were men. Preoperatively, 361 of 710 (50.8%) of patients were in New York Heart Association class III or IV, and at 6 years postoperatively, 92 of 96 (95.8%) were New York Heart Association class I or II. Six years postoperatively, average mean gradient across all valve sizes was 11.0 mm Hg, and the average effective orifice area index was 0.80 cm2/m2. The proportion of patients without moderate-to-severe valvular regurgitation at 6 years was 95.2% (80/84). Six years postoperatively, freedom from valve-related mortality, nonstructural dysfunction, and paravalvular leak were 98.3%, 98.6%, and 98.9%, respectively, and freedom from reoperation due to structural valve deterioration was 97.3% (95% confidence limits, 98.6-94.7).ConclusionThese midterm results demonstrate that the Trifecta valve is a safe and effective valve substitute with excellent hemodynamic performance and durability that is maintained through the 6-year follow-up period.

Background: Paravalvular leak (PVL) after transcatheter aortic valve implantation (TAVI) is frequent and the impact of mild PVL on outcomes remains uncertain. Our study aimed to evaluate the impact of PVL on TAVI outcomes. Methods: To analyze late outcomes of patients after TAVI according to the presence and severity of PVL, PubMed/MEDLINE, EMBASE and Google Scholar were searched for studies that reported rates of all-cause mortality/survival and/or rehospitalization and/or cardiovascular mortality accompanied by at least one Kaplan-Meier curve for any of these outcomes. We adopted a 2-stage approach to reconstruct individual patient data based on the published Kaplan-Meier graphs. Results: < 0.001) during follow-up. Conclusions: Patients with PVL, even if mild, experience higher risk of all-cause mortality, rehospitalization, and cardiovascular mortality following TAVI. These findings provide support to the implementation of procedural strategies to prevent any degree of PVL at the time of TAVI.

BACKGROUND: Erectile dysfunction (ED) may be one manifestation of a generalized vascular disorder characterized by endothelial dysfunction. Statin drugs may improve endothelial function, even before altering the lipid profile. OBJECTIVE: We sought to determine whether the addition of a statin with sildenafil would improve ED in men who initially responded poorly to sildenafil. METHODS: Men with moderate-to-severe ED despite an adequate sildenafil trial were enrolled in this randomized, double-blind, placebo-controlled pilot study. ED was defined using a validated self-administered questionnaire as a score of <or=16 on the International Index of Erectile Function (erectile function domain score range of 6-30). Improvement in ED score with sildenafil was reassessed at 6 and 12 weeks of treatment with atorvastatin (80 mg daily) or matching placebo. RESULTS: Twelve men (mean age 58 +/- 13 years) with a mean domain score of 8.2 +/- 6.9 and a mean duration of ED of 3.7 years were enrolled in the study. Treatment with atorvastatin decreased mean low-density lipoprotein cholesterol by 43% and resulted in an improvement with sildenafil in domain score of 7.8 (P = 0.036); an effect was apparent by 6 weeks. The increase in domain score in placebo patients was not statistically significant. CONCLUSIONS: Treatment with atorvastatin improved sexual function and the response to oral sildenafil in men who did not initially respond to treatment with sildenafil. The results of this pilot study support the hypothesis that vascular endothelial dysfunction contributes to ED in sildenafil nonresponders and deserves further testing in a large clinical trial.

Aims: The presence of cancer can complicate treatment choices for patients with atrial fibrillation (AF) increasing both the risk of thrombotic and bleeding events. Methods and results: Using data from Outcomes Registry for Better Informed Treatment of Atrial Fibrillation, we aimed to characterize AF patients with cancer, to describe their management and to assess the association between cancer and cardiovascular (CV) outcomes. Among 9749 patients, 23.8% had history of cancer (57% solid malignancy, 1.3% leukaemia, 3.3% lymphoma, 40% other type, and 2.2% metastatic cancer). Patients with history of cancer were older, more likely to have CV disease, CV risk factors, and prior gastrointestinal bleeding. No difference in antiarrhythmic and antithrombotic therapy was observed between those with and without cancer. Patients with history of cancer had a significantly higher risk of death (7.8 vs. 4.9 deaths per 100 patient-years follow-up, P = 0.0003) mainly driven by non-CV death (4.2 vs. 2.4 per 100 patient-years follow-up; P = 0.0004) and higher risk of major bleeding (5.1 vs. 3.5 per 100 patient-years follow-up; P = 0.02) compared with non-cancer patients; no differences were observed in risks of strokes/non-central nervous system embolism (1.96 vs. 1.48, P = 0.74) and CV death (2.89 vs. 2.07, P = 0.35) between the two groups. Conclusion: A history of cancer is common among AF patients with up to one in four patients having both. Antithrombotic therapy, rates of cerebrovascular accident, other thrombotic events and cardiac death were similar in AF patients with or without a history of cancer. Patients with cancer, however, were at higher risk of major bleeding and non-CV death.

BACKGROUND: COVID-19 is a respiratory infectious disease caused by SARS-CoV-2, and cardiovascular damage is commonly observed in affected patients. We sought to investigate the effect of SARS-CoV-2 infection on cardiac injury and hypertension during the current coronavirus pandemic. STUDY DESIGN AND METHODS: The clinical data of 366 hospitalized COVID-19-confirmed patients were analyzed. The clinical signs and laboratory findings were extracted from electronic medical records. Two independent, experienced clinicians reviewed and analyzed the data. RESULTS: Cardiac injury was found in 11.19% (30/268) of enrolled patients. 93.33% (28/30) of cardiac injury cases were in the severe group. The laboratory findings indicated that white blood cells, neutrophils, procalcitonin, C-reactive protein, lactate, and lactic dehydrogenase were positively associated with cardiac injury marker. Compared with healthy controls, the 190 patients without prior hypertension have higher AngⅡ level, of which 16 (8.42%) patients had a rise in blood pressure to the diagnostic criteria of hypertension during hospitalization, with a significantly increased level of the cTnI, procalcitonin, angiotensin-II (AngⅡ) than those normal blood pressure ones. Multivariate analysis indicated that elevated age, cTnI, the history of hypertension, and diabetes were independent predictors for illness severity. The predictive model, based on the four parameters and gender, has a good ability to identify the clinical severity of COVID-19 in hospitalized patients (area under the curve: 0.932, sensitivity: 98.67%, specificity: 75.68%). CONCLUSION: Hypertension, sometimes accompanied by elevated cTnI, may occur in COVID-19 patients and become a sequela. Enhancing Ang II signaling, driven by SARS-CoV-2 infection, might play an important role in the renin-angiotensin system, and consequently lead to the development of hypertension in COVID-19.

OBJECTIVES: The purpose of this study was to prospectively assess the effect of dynamic cardiomyoplasty in patients with symptomatic chronic heart failure. BACKGROUND: Since the first procedure was performed in 1985, dynamic cardiomyoplasty has been developed for use in patients with chronic heart failure. The aging population in developed countries has made heart failure a growing public health concern. Heart transplantation is appropriate or available for only a small proportion of these patients because of limited donor supply. Effective alternatives to transplantation are needed. METHODS: Eight centers in North and South America performed 68 cardiomyoplasty procedures between May 1991 and September 1993. Data were prospectively collected every 6 months and compared with preoperative values using paired t tests, chi-square tests and actuarial survival analyses. RESULTS: Patients had a mean (+/- SD) age of 57 +/- 1 years and were predominantly male (53 [78%] of 68). Heart failure etiology was classified as idiopathic in 47 (69%) of 68 patients and ischemic in 21 (31%). The in-hospital mortality rate was 12% (8 of 68), and the survival rate at 6 and 12 months was 75 +/- 5% and 68 +/- 6%, respectively. Objective improvements were seen at 6 months (n = 49) in left ventricular ejection fraction (23 +/- 1% vs. 25 +/- 1%, p = 0.05), stroke volume (50 +/- 2 vs. 56 +/- 3 ml/beat, p = 0.02) and left ventricular stroke work index (26 +/- 1 vs 30 +/- 2 g/m2 per beat, p = 0.01). Improvements in mean New York Heart Association functional class (3 +/- 0.04 vs. 1.8 +/- 0.1, p = 0.0001) and activity of daily living score (59 +/- 3 vs. 80 +/- 2, p = 0.0001) were also observed. There were no significant changes at 6 months in peak oxygen consumption (15 +/- 1 vs. 16 +/- 1 ml/kg per min), cardiac index (2.26 +/- 0.08 vs. 2.33 +/- 0.08 liters/min per m2), pulmonary capillary wedge pressure (19 +/- 2 vs. 18 +/- 1 mm Hg) or heart rate (87 +/- 2 vs. 82 +/- 3 beats/min). CONCLUSIONS: These data suggest that dynamic cardiomyoplasty improves ventricular systolic function, reduces symptoms of heart failure and improves objective measures of quality of life in patients with congestive heart failure. This improvement occurred without changes in peak exercise capacity, ventricular filling pressure or actuarial survival.

Background: A recent summary-level meta-analysis comprising randomized, controlled trials (RCTs) of femoropopliteal paclitaxel-coated balloon and stent intervention identified excess late mortality in the paclitaxel-treated patients. Methods: We evaluated the safety of the Stellarex drug-coated balloon (DCB) for femoropopliteal artery disease with an independently performed meta-analysis of patient-level data from all patients in the Stellarex femoropopliteal clinical program. To compare mortality after DCB or uncoated percutaneous transluminal angioplasty (PTA), we aggregated data from 2 RCTs comprising 419 patients treated with DCB and 170 patients treated with PTA. In an additional analysis, data were aggregated from 6 poolable Stellarex DCB studies (2 RCTs, 3 single-arm studies, and 1 registry). All serious adverse events including deaths were adjudicated by a blinded, third-party, independent Clinical Events Committee. Kaplan–Meier estimates in the RCTs were compared with restricted mean survival time. Predictors of death were assessed with hazard ratios (HRs) and Cox proportional hazards modeling. Results: Baseline characteristics were similar in the patients treated with DCB and PTA in the pooled RCT analysis, with the exception that the DCB cohort was younger (67.4±9.7 versus 69.4±9.4 years, P =0.02), smoked more frequently (86.6% versus 78.8%, P =0.02), and were less often treated for recurrent lesions (8.8% versus 14.7%, P =0.04). In the RCTs, patients treated with DCB had all-cause mortality rates that were not different from those of patients treated with PTA (Kaplan–Meier estimates 1.8±0.7% versus 1.3±0.9%, 6.5±1.2% versus 5.9±1.9%, and 9.3±1.5% versus 9.9±2.4% at 1, 2, and 3 years, respectively, P =0.86). All-cause mortality rates were similar in a 1906-patient pooled nonrandomized DCB data set (Kaplan–Meier estimates of 2.1%, 4.9%, and 7.0% at 1, 2, and 3 years, respectively). Clinical Events Committee–adjudicated causes of death were balanced between the DCB and PTA cohorts. Multivariable Cox modeling identified age (HR, 1.06; 95% CI, 1.04–1.08; P &lt;0.001), diabetes mellitus (HR, 1.42; 95% CI, 1.01–2.00; P =0.04), congestive heart failure (HR, 1.88; 95% CI, 1.12–3.16; P =0.02), and renal insufficiency (HR, 2.00; 95% CI, 1.33–3.01; P &lt;0.001) as predictors of mortality. Paclitaxel exposure was unrelated to mortality (HR, 1.04; 95% CI, 0.98–1.10; P =0.23). Conclusions: The mortality rates for patients treated with the DCB and uncoated PTA were indistinguishable over 3-year follow-up. Additional patient-level, adequately powered meta-analyses with larger RCT data sets will be needed to confirm the generalizability of these findings. Clinical Trial Registration: URL: http://www.clinicaltrials.gov . Unique identifiers: NCT02110524, NCT01858363, NCT01858428, NCT03421561, NCT01912937, NCT01927068, and NCT02769273.

Sophisticated diagnostic information is provided by the latest generation of implantable defibrillators. The success of therapy and the type of therapy successful in terminating ventricular arrhythmias is provided by interrogating the ICD device. In addition, R to R interval information can be retrieved. In selected devices, either local bipolar electrograms from the rate sensing leads or wide bipolar electrograms from the energy delivering leads provide visual confirmation of the presence of ventricular tachyarrthythmic events leading to therapy. The value and limitations of this sophisticated diagnostic information in providing insight into the electrical events triggering therapy and the events triggering ventricular arrhythmias are discussed.