Suture closure AFtEr large bore vein access (SAFE-VEIN): A randomized, prospective study of the efficacy and safety of venous closure device.

BACKGROUND: Perclose ProGlide (PPG) Suture-Mediated Closure System™ is safe and can reduce time to hemostasis following procedures requiring arterial access. AIMS: We aimed to compare PPG to figure of 8 suture in patients who underwent interventional catheter procedures requiring large bore venous access (LBVA) (≥13 French). METHODS: In this physician-initiated, randomized, single-center study [clinicaltrials.gov ID: NCT04632641], single-stick venous access was obtained under ultrasound guidance. Eligible patients were randomized 1:1, and 100 subjects received allocated treatment to either PPG (n = 47) or figure of 8 suture (n = 53). No femoral arterial access was used in any patient. Primary outcomes were time to achieve hemostasis (TTH) and time to ambulation (TTA). Secondary outcomes were time to discharge (TTD) and vascular-related complications and mortality. Wilcoxon rank-sum test was used to compare TTH, TTA, and TTD. RESULTS: TTH (minutes) was significantly lower in PPG versus figure of 8 suture [median, (Q1, Q3)] [7 (2,10) vs. 11 (10,15) respectively, p < 0.001]. TTA (minutes) was significantly lower in PPG compared to figure of 8 suture [322 (246,452) vs. 403 (353, 633) respectively, p = 0.005]. TTD (minutes) was not significantly different between the PPG and figure of 8 suture arms [1257 (1081, 1544) vs. 1338 (1171,1435), p = 0.650]. There was no difference in minor bleeding or access site hematomas between both arms. No other vascular complications or mortality were reported. CONCLUSION: PPG use had lower TTH and TTA than figure of 8 suture in a population of patients receiving LBVA procedures. This may encourage same-day discharge in these patients.

In adults aged 75 to 76 y, systematic AF screening reduced morbidity and mortality at 6 y.

SOURCE CITATION: Svennberg E, Friberg L, Frykman V, et al. Clinical outcomes in systematic screening for atrial fibrillation (STROKESTOP): a multicentre, parallel group, unmasked, randomised controlled trial. Lancet. 2021;398:1498-1506. 34469764.

In older patients at high risk for stroke, intensive AF screening with an implantable loop recorder did not reduce stroke.

SOURCE CITATION: Svendsen JH, Diederichsen SZ, Højberg S, et al. Implantable loop recorder detection of atrial fibrillation to prevent stroke (The LOOP Study): a randomised controlled trial. Lancet. 2021;398:1507-16. 34469766.

Aging-associated susceptibility to stress-induced ventricular arrhythmogenesis is attenuated by tetrodotoxin.

Aging is associated with increased prevalence of life-threatening ventricular arrhythmias, but mechanisms underlying higher susceptibility to arrhythmogenesis and means to prevent such arrhythmias under stress are not fully defined. We aimed to define differences in aging-associated susceptibility to ventricular fibrillation (VF) induction between young and aged hearts. VF induction was attempted in isolated perfused hearts of young (6-month) and aged (24-month-old) male Fischer-344 rats by rapid pacing before and following isoproterenol (1 µM) or global ischemia and reperfusion (I/R) injury with or without pretreatment with low-dose tetrodotoxin, a late sodium current blocker. At baseline, VF could not be induced; however, the susceptibility to inducible VF after isoproterenol and spontaneous VF following I/R was 6-fold and 3-fold higher, respectively, in old hearts (P < 0.05). Old animals had longer epicardial monophasic action potential at 90% repolarization (APD90; P < 0.05) and displayed a loss of isoproterenol-induced shortening of APD90 present in the young. In isolated ventricular cardiomyocytes from older but not younger animals, 4-aminopyridine prolonged APD and induced early afterdepolarizations (EADs) and triggered activity with isoproterenol. Low-dose tetrodotoxin (0.5 µM) significantly shortened APD without altering action potential upstroke and prevented 4-aminopyridine-mediated APD prolongation, EADs, and triggered activity. Tetrodotoxin pretreatment prevented VF induction by pacing in isoproterenol-challenged hearts. Vulnerability to VF following I/R or catecholamine challenge is significantly increased in old hearts that display reduced repolarization reserve and increased propensity to EADs, triggered activity, and ventricular arrhythmogenesis that can be suppressed by low-dose tetrodotoxin, suggesting a role of slow sodium current in promoting arrhythmogenesis with aging.

Risk of Atrial Fibrillation and Stroke After Bariatric Surgery in Patients With Morbid Obesity With or Without Obstructive Sleep Apnea.

Background and Purpose: Weight loss in morbidly obese patients reduces atrial fibrillation (AF); however, it is unknown whether similar benefits are maintained in patients with obstructive sleep apnea (OSA). We sought to determine whether incident AF and stroke rates are affected by OSA after weight loss and to identify predictors of AF and stroke. Methods: Differences in laparoscopic adjustable gastric banding­induced weight loss on incident AF and stroke events in those with and without OSA in the entire and in propensity-matched cohorts were determined longitudinally, and independent predictors of AF and stroke were identified. Results: Of 827 morbidly obese patients who underwent laparoscopic adjustable gastric banding (mean age, 44±11 years; mean body mass index, 49±8 kg/m2), incident AF was documented in 4.96% and stroke in 5.44% of patients during a mean 6.0±3.2-year follow-up. Despite a similar reduction in body weight (19.6% and 21% in 3 years), new-onset AF was significantly higher in patients with OSA than without OSA in the entire (1.7% versus 0.5% per year; P<0.001) and propensity-matched cohorts. Incident stroke was higher in the OSA than in the non-OSA group (2.10% versus 0.47% per year; P<0.001), but only 20% of patients with stroke had documented AF. On multivariate analysis, OSA (hazard ratio, 2.88 [95% CI, 1.45­5.73]), age, and hypertension were independent predictors of new-onset AF, and OSA (hazard ratio, 5.84 [95% CI, 3.02­11.30]), depression, and body mass index were for stroke events. Conclusions: In morbidly obese patients who underwent laparoscopic adjustable gastric banding, despite similar weight loss, patients with OSA had a higher incidence of AF and stroke than patients without OSA. Both non-AF and AF-related factors were involved in increasing stroke risk. Further investigation is warranted into whether OSA treatment helps reduce AF or stroke events in this population.

Prolonged post-differentiation culture influences the expression and biophysics of Na+ and Ca2+ channels in induced pluripotent stem cell-derived ventricular-like cardiomyocytes.

Several studies have been reported in various domains from induction methods to utilities of somatic cell pluripotent reprogramming. However, one of the major struggles facing the research field of induced pluripotent stem cell (iPSC)-derived target cells is the lack of consistency in observations. This could be due to variety of reasons including varied culture periods post-differentiation. The cardiomyocytes (CMs) derived from iPSCs are commonly studied and proposed to be utilized in the comprehensive in vitro proarrhythmia initiative for drug safety screening. As the influence of varied culture periods on the electrophysiological properties of iPSC-CMs is not clearly known, using whole-cell patch clamp technique, we compared two groups of differentiated ventricular-like iPSC-CMs that are cultured for 10 to 15 days (D10-15) and more than 30 days (≥ D30) both under current and voltage clamps. The prolonged culture imparts increased excitability with high-frequency spontaneous action potentials, robust increase in the magnitude of peak Na+ current density, relatively shallow inactivation kinetics of Na+ channels, faster recovery from inactivation, and augmented Ca2+ current density. Quantitative real-time PCR studies of α-subunit transcripts showed enhanced mRNA expression of SCN1A, SCN5A Na+ channel subtypes, and CACNA1C, CACNA1G, and CACNA1I Ca2+ channel subtypes, in ≥ D30 group. Conclusively, the prolonged culture of differentiated iPSC-CMs affects the excitability, single-cell electrophysiological properties, and ion channel expressions. Therefore, following standard periods of culture across research studies while utilizing ventricular-like iPSC-CMs for in vitro health/disease modeling to study cellular functional mechanisms or test high-throughput drugs' efficacy and toxicity becomes crucial.

Contemporary practice pattern of revascularization in a large tertiary care referral center in non-ST elevation myocardial infarction: A propensity-matched 10-year experience.

OBJECTIVES: We sought to compare the effects of early versus delayed percutaneous coronary intervention (PCI) on the outcomes at 1 year in patients presenting with non-ST-segment elevation myocardial infarction (NSTEMI). BACKGROUND: Prompt reperfusion in NSTEMI remains controversial. Randomized studies have shown conflicting results regarding the benefits of early intervention versus delayed intervention (defined as intervention performed within 24 hr vs. 24-72 hr of presentation, respectively). This study was conducted to determine the clinical outcomes post PCI in a large tertiary care center. METHODS: A propensity-matched group of 1,640 NSTEMI patients [62.4% males (n = 1,023), median age 65 years] was studied for a composite of death, myocardial infarction (MI), stroke, and heart failure in 1 year as a primary endpoint after PCI. Patients were divided into an early intervention group (EIG) and delayed intervention group (DIG). Timing of PCI was determined by the treating interventional cardiologist. RESULTS: The primary outcome was significantly lower in the EIG than DIG (20.4% vs. 24.9%, P = 0.029), which was mainly derived from mortality benefit in the EIG. There was no difference in occurrence of death, MI, stroke, or heart failure between the groups at 30 days. CONCLUSIONS: An earlier PCI in patients with NSTEMI is associated with a significant reduction in the composite outcome of death, MI, heart failure, or stroke at 1 year compared with delayed PCI. Based on this large cohort of patients from a real-world referral center, contemporary reperfusion practices in NSTEMI may need to be re-examined with a bias toward early intervention.

Prioritizing Functional Capacity as a Principal End Point for Therapies Oriented to Older Adults With Cardiovascular Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association.

Adults are living longer, and cardiovascular disease is endemic in the growing population of older adults who are surviving into old age. Functional capacity is a key metric in this population, both for the perspective it provides on aggregate health and as a vital goal of care. Whereas cardiorespiratory function has long been applied by cardiologists as a measure of function that depended primarily on cardiac physiology, multiple other factors also contribute, usually with increasing bearing as age advances. Comorbidity, inflammation, mitochondrial metabolism, cognition, balance, and sleep are among the constellation of factors that bear on cardiorespiratory function and that become intricately entwined with cardiovascular health in old age. This statement reviews the essential physiology underlying functional capacity on systemic, organ, and cellular levels, as well as critical clinical skills to measure multiple realms of function (eg, aerobic, strength, balance, and even cognition) that are particularly relevant for older patients. Clinical therapeutic perspectives and patient perspectives are enumerated to clarify challenges and opportunities across the caregiving spectrum, including patients who are hospitalized, those managed in routine office settings, and those in skilled nursing facilities. Overall, this scientific statement provides practical recommendations and vital conceptual insights.

Aging-related increase in store-operated Ca2+ influx in human ventricular fibroblasts.

Senescence-related fibrosis contributes to cardiac dysfunction. Profibrotic processes are Ca2+ dependent. The effect of aging on the Ca2+ mobilization processes of human ventricular fibroblasts (hVFs) is unclear. Therefore, we tested whether aging altered intracellular Ca2+ release and store-operated Ca2+ entry (SOCE). Disease-free hVFs from 2- to 63-yr-old trauma victims were assessed for cytosolic Ca2+ dynamics with fluo 3/confocal imaging. Angiotensin II or thapsigargin was used to release endoplasmic reticulum Ca2+ in Ca2+-free solution; CaCl2 (2 mM) was then added to assess SOCE, which was normalized to ionomycin-induced maximal Ca2+. The angiotensin II experiments were repeated after phosphoenolpyruvate pretreatment to determine the role of energy status. The expression of genes encoding SOCE-related ion channel subunits was assessed by quantitative PCR, and protein expression was assessed by immunoblot analysis. Age groups of <50 and ≥50 yr were compared using unpaired t-test or regression analysis. Ca2+ release by angiotensin II or thapsigargin was not different between the groups, but SOCE was significantly elevated in the ≥50-yr group. Regression analysis showed an age-dependent phosphoenolpyruvate-sensitive increase in SOCE of hVFs. Aging did not alter the mRNA expression of SOCE-related genes. The profibrotic phenotype of hVFs was evident by sprouty1 downregulation with age. Thus, an age-associated increase in angiotensin II- and thapsigargin-induced SOCE occurs in hVFs, independent of receptor mechanisms or alterations of mRNA expression level of SOCE-related ion channel subunits but related to the cellular bioenergetics status. Elucidation of mechanisms underlying enhanced hVF SOCE with aging may refine SOCE targets to limit aging-related progression of Ca2+-dependent cardiac fibrosis. NEW & NOTEWORTHY Human ventricular fibroblasts exhibit an age-related increase in store-operated Ca2+ influx induced by angiotensin II, an endogenous vasoactive hormone, or thapsigargin, an inhibitor of endoplasmic reticulum Ca2+-ATPase, independent of receptor mechanisms or genes encoding store-operated Ca2+ entry-related ion channel subunits. Selective inhibition of this augmented store-operated Ca2+ entry could therapeutically limit aging-related cardiac fibrosis.

Bivalirudin versus unfractionated heparin during peripheral vascular interventions: A Propensity-matched Study.

OBJECTIVES: This study aimed to compare the association of access site complications and the use of unfractionated heparin versus bivalirudin during subinguinal peripheral vascular intervention. BACKGROUND: Compared to unfractionated heparin, bivalirudin has been associated with fewer bleeding complications in patients undergoing percutaneous coronary intervention but more ischemic events. The safety and efficacy of direct thrombin inhibitors in peripheral vascular interventions is not well defined. METHODS: We compared the incidence of in-hospital access site complications and discharge status among patients in the multicenter, prospective Vascular Quality Initiative registry who underwent peripheral vascular intervention between August 2007 and January 2014 using bivalirudin or unfractionated heparin. Propensity score matching was used to obtain a balanced cohort of 1,524 patients in each treatment group. RESULTS: Patients treated with bivalirudin had a significantly lower incidence of access site hematomas (2.4% vs. 3.9%, P = 0.018), shorter post-procedural hospitalization (1.0 vs. 1.2 days, P < 0.001) and lower rates of discharge to a nursing home or rehabilitation center rather than home (7.61% vs. 9.73%, P = 0.034) when compared with unfractionated heparin-treated patients. The incidence of in-hospital access site occlusion, distal embolization, and mortality did not differ significantly between groups. CONCLUSIONS: Patients who received bivalirudin had lower rates of access site hematoma, shorter length of stay, and improved discharge status compared with unfractionated heparin during hospitalization for peripheral vascular intervention. Randomized comparisons of these agents are needed to confirm these findings. © 2016 Wiley Periodicals, Inc.

Harnessing the Power of Integrated Mitochondrial Biology and Physiology: A Special Report on the NHLBI Mitochondria in Heart Diseases Initiative.

Mitochondrial biology is the sum of diverse phenomena from molecular profiles to physiological functions. A mechanistic understanding of mitochondria in disease development, and hence the future prospect of clinical translations, relies on a systems-level integration of expertise from multiple fields of investigation. Upon the successful conclusion of a recent National Institutes of Health, National Heart, Lung, and Blood Institute initiative on integrative mitochondrial biology in cardiovascular diseases, we reflect on the accomplishments made possible by this unique interdisciplinary collaboration effort and exciting new fronts on the study of these remarkable organelles.

Chamber-specific differences in human cardiac fibroblast proliferation and responsiveness toward simvastatin.

Fibroblasts, the most abundant cells in the heart, contribute to cardiac fibrosis, the substrate for the development of arrythmogenesis, and therefore are potential targets for preventing arrhythmic cardiac remodeling. A chamber-specific difference in the responsiveness of fibroblasts from the atria and ventricles toward cytokine and growth factors has been described in animal models, but it is unclear whether similar differences exist in human cardiac fibroblasts (HCFs) and whether drugs affect their proliferation differentially. Using cardiac fibroblasts from humans, differences between atrial and ventricular fibroblasts in serum-induced proliferation, DNA synthesis, cell cycle progression, cyclin gene expression, and their inhibition by simvastatin were determined. The serum-induced proliferation rate of human atrial fibroblasts was more than threefold greater than ventricular fibroblasts with faster DNA synthesis and higher mRNA levels of cyclin genes. Simvastatin predominantly decreased the rate of proliferation of atrial fibroblasts, with inhibition of cell cycle progression and an increase in the G0/G1 phase in atrial fibroblasts with a higher sensitivity toward inhibition compared with ventricular fibroblasts. The DNA synthesis and mRNA levels of cyclin A, D, and E were significantly reduced by simvastatin in atrial but not in ventricular fibroblasts. The inhibitory effect of simvastatin on atrial fibroblasts was abrogated by mevalonic acid (500 µM) that bypasses 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition. Chamber-specific differences exist in the human heart because atrial fibroblasts have a higher proliferative capacity and are more sensitive to simvastatin-mediated inhibition through HMG-CoA reductase pathway. This mechanism may be useful in selectively preventing excessive atrial fibrosis without inhibiting adaptive ventricular remodeling during cardiac injury.

Selective downregulation of mitochondrial electron transport chain activity and increased oxidative stress in human atrial fibrillation.

Mitochondria are critical for maintaining normal cardiac function, and a deficit in mitochondrial energetics can lead to the development of the substrate that promotes atrial fibrillation (AF) and its progression. However, the link between mitochondrial dysfunction and AF in humans is still not fully defined. The aim of this study was to elucidate differences in the functional activity of mitochondrial oxidative phosphorylation (OXPHOS) complexes and oxidative stress in right atrial tissue from patients without (non-AF) and with AF (AF) who were undergoing open-heart surgery and were not significantly different for age, sex, major comorbidities, and medications. The overall functional activity of the electron transport chain (ETC), NADH:O2 oxidoreductase activity, was reduced by 30% in atrial tissue from AF compared with non-AF patients. This was predominantly due to a selective reduction in complex I (0.06 ± 0.007 vs. 0.09 ± 0.006 nmol·min(-1)·citrate synthase activity(-1), P = 0.02) and II (0.11 ± 0.012 vs. 0.16 ± 0.012 nmol·min(-1)·citrate synthase activity(-1), P = 0.003) functional activity in AF patients. Conversely, complex V activity was significantly increased in AF patients (0.21 ± 0.027 vs. 0.12 ± 0.01 nmol·min(-1)·citrate synthase activity(-1), P = 0.005). In addition, AF patients exhibited a higher oxidative stress with increased production of mitochondrial superoxide (73 ± 17 vs. 11 ± 2 arbitrary units, P = 0.03) and 4-hydroxynonenal level (77.64 ± 30.2 vs. 9.83 ± 2.83 ng·mg(-1) protein, P = 0.048). Our findings suggest that AF is associated with selective downregulation of ETC activity and increased oxidative stress that can contribute to the progression of the substrate for AF.

Hypertrophic Cardiomyopathy-Septal Perforator Arteries Doppler Flow Dynamics.

BACKGROUND: Patients with hypertrophic cardiomyopathy (HCM) have been shown to exhibit abnormal diastolic vessel flow; however, flow pattern profiles and their possible association with different grades of diastolic dysfunction have not been studied. Color Doppler two-dimensional echocardiography permits visualization of the septal perforator arteries, and pulsed-wave Doppler allows recording of diastolic septal artery flow (SAF). Through routine visualization of the septal perforator arteries and acquisition of SAF, we noticed 3 patterns of SAF in patients with HCM. In this study, we aimed to assess the feasibility of the acquisition of SAF and to describe types of SAF in an HCM cohort and their associations with diastolic function. METHODS: We reviewed two-dimensional echocardiograms and the electronic records of 108 patients with HCM in whom septal artery color and spectral Doppler had been performed. The peak diastolic and end-diastolic velocities, diastolic slope, diastolic flow time-velocity integral, and systolic flow reversal of the septal perforator arteries were recorded with pulsed-wave Doppler. Echocardiographic and clinical characteristics were analyzed. RESULTS: A reproducible pulsed-wave Doppler tracing was recorded in 54% of patients with HCM. Three distinct patterns of SAF were identified: type 1-smooth, linear holodiastolic velocity decrease; type 2-with presence of an atrial dip; and type 3-biphasic velocity decrease with an early, rapid diastolic slope and a mid-to-late gentle slope. These 3 SAFs correlated with different grades of diastolic dysfunction. CONCLUSION: Septal artery flow could be detected in more than 50% of patients with HCM. Three distinct types of SAF were identified, correlating with different grades of diastolic dysfunction. These 3 types of SAF can provide additional information about left ventricular end-diastolic pressure and diastolic function in patients with HCM in whom diastolic function may be difficult to determine.

Clinical Interpretation of Genetic Variants in the Evaluation and Management of Thoracic Aortic Aneurysm and Dissection.

BACKGROUND: We aimed to elucidate clinical implications of genetic variant interpretation in assessing disease severity and progression in thoracic aortic aneurysm and dissection (TAAD) patients. METHODS: Consecutive TAAD patients with aortic root and/or ascending aortic aneurysms seen between 2011 and 2020 were included. Serial echocardiography, family history of TAAD, and management information were retrospectively collected and analyzed. Patients were classified into gene-positive (Gen-P), variants of uncertain significance, and gene-negative (Gen-N) groups. RESULTS: A total of 407 patients were included: mean age 53.7 ± 15.4 years, 64.4% men, and 38% with reported family history of TAAD. Thirty-seven (9.1%) were Gen-P; 147 (36.1%) had a variant of uncertain significance. The maximal aneurysm diameter was 4.78 mm larger in Gen-P than the other groups (P < .001). In 162 unoperated TAAD patients with serial echocardiographic measurements, aneurysms enlarged at a significantly higher rate in the Gen-P (1.36 mm/year, 95% CI: 0.77-1.95) than variants of uncertain significance and Gen-N groups (0.83 mm/year vs 0.89 mm/year, respectively; P < .001). Aneurysms were 20% more likely to require surgical intervention for every millimeter increase in diameter. When considered on an individual basis, the highest growth rates were found in the variants of uncertain significance group. CONCLUSIONS: While aneurysms linked to variants of uncertain significance demonstrate average growth rates comparable to those in Gen-N, close follow-up and genetic counseling in the variants of uncertain significance group are recommended for assessment of pathogenicity on a case-by-case basis. Early familial gene testing in TAAD is important to develop individualized preventive and therapeutic criteria.

The Uncertain Benefit from Implantable Cardioverter-Defibrillators in Nonischemic Cardiomyopathy: How to Guide Clinical Decision-Making?

Life-threatening dysrhythmias remain a significant cause of mortality in patients with nonischemic cardiomyopathy (NICM). Implantable cardioverter-defibrillators (ICD) effectively reduce mortality in patients who have survived a life-threatening arrhythmic event. The evidence for survival benefit of primary prevention ICD for patients with high-risk NICM on guideline-directed medical therapy is not as robust, with efficacy questioned by recent studies. In this review, we summarize the data on the risk of life-threatening arrhythmias in NICM, the recommendations, and the evidence supporting the efficacy of primary prevention ICD, and highlight tools that may improve the identification of patients who could benefit from primary prevention ICD implantation.

Age-Based Outcomes in Patients Who Underwent Septal Reduction Therapy.

There are no national data on age-based outcomes of septal reduction therapy. Using the National Inpatient Sample, we included all adult patients who underwent septal myectomy (SM) or alcohol septal ablation (ASA) from 2005 to 2019. The primary objective was to evaluate the in-hospital mortality and new permanent pacemaker (PPM) placement after SM and ASA in 3 age groups. In total, 9,564 patients underwent SM and 5,084 underwent ASA. Compared with the age group 18 to 39 years, the odds of in-hospital mortality after SM were similar in age group 40 to 64 years and 4.46 times higher than in age group ≥65 years; the higher mortality in the older group was explained by higher co-morbidity burden on the risk-adjusted analysis. Furthermore, compared with age group 18 to 39 years, the odds of new PPM placement after SM were higher in the age groups 40 to 64 years and ≥65 years, despite the risk adjustment (adjusted odds ratio [AOR] 3.17, 95% confidence interval [CI] 1.33 to 7.58 and AOR 4.39, 95% CI 1.78 to 10.8, respectively). The odds of in-hospital mortality after ASA were similar in age groups 65 to 79 years and 18 to 64 years. However, the odds of in-hospital mortality were higher in the age group ≥80 years than in the age group 18 to 64 years, although this difference were not present after risk adjustment. The odds of new PPM after ASA were higher for the age groups 65 to 79 years and ≥80 years than age group 18 to 64 years, despite the risk adjustment (AOR 1.78, 95% CI 1.22 to 2.60 and AOR 3.10, 95% CI 2.09 to 6.57, respectively). Finally, we also estimated these absolute risks in different age groups. In conclusion, this national data will inform health care providers to better understand the aged-based risks of outcomes after septal reduction therapy.

Regional Disparities in the Use of Septal Reduction Therapy and Associated Outcomes in the United States (from a Real-World Database).

The regional differences in the use of septal reduction therapies and the associated outcomes in patients with Hypertrophic obstructive cardiomyopathy (HOCM) are unknown. The primary objective of our study was to evaluate the regional disparities in the use of septal reduction therapies, including septal myectomy and alcohol septal ablation, in patients with HOCM. The secondary objective was to analyze the regional differences in the outcomes in these patients. Patients with HOCM had 87% higher risk-adjusted odds of getting septal myectomy (adjusted odds ratio 1.87, p = 0.03) and 37% lower risk-adjusted odds of getting alcohol septal ablation (adjusted odds ratio 0.63, p = 0.03) in the Midwest than in the Northeast. The in-hospital mortality rate was higher for patients who underwent septal myectomy in the South versus the Northeast on the unadjusted analysis. These differences persisted despite the adjustment for demographic and clinical characteristics. Additional adjustment for hospital volume partially explained these disparities, but the adjustment for both hospital volume and hospital teaching status completely explained these disparities. The risk-adjusted in-hospital mortality in patients who underwent alcohol septal ablation was similar in the South versus other regions. In conclusion, regional disparities may exist in the use of septal myectomy and alcohol septal ablation, and patients with HOCM should be referred to high-volume teaching hospitals for septal myectomy for better outcomes, which may also eliminate the extra burden of hospital mortality in the South.