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Bandyopadhyay D, Chakraborty S, Amgai B, et al. Association of Hypertrophic Obstructive Cardiomyopathy With Outcomes Following Transcatheter Aortic Valve Replacement. JAMA Netw Open. 2020;3(2):e1921669. doi:10.1001/jamanetworkopen.2019.21669
Hypertrophic cardiomyopathy (HCM) and valvular aortic stenosis can both present with left ventricular outflow obstruction and hypertrophy. In patients with aortic stenosis and coexisting HCM undergoing transcatheter aortic valve replacement (TAVR), this can pose a management dilemma, as one condition can modulate the effects of the other. Indeed, there has been anecdotal concern that treating the aortic valve prior to treating outflow tract obstruction may result in higher mortality due to exacerbation of subvalvular obstruction. There are limited data on optimal management or outcomes of coexisting HCM and aortic stenosis in patients who undergo TAVR. We conducted a retrospective cohort study using the National Inpatient Sample to identify the association of known HCM with outcomes following TAVR.
We queried the 2012 to 2016 National Inpatient Sample to identify all patients (aged ≥18 years) who underwent TAVR and had coexisting HCM by using respective International Classification of Diseases, Ninth Edition, Clinical Modification (ICD-9-CM) or International Statistical Classification of Diseases, Tenth Revision, Clinical Modification Procedure Coding System (ICD-10-CM/PCS) codes. Our primary outcome was in-hospital mortality. Categorical data were presented as counts and percentages, and continuous data as means with standard deviations or standard errors. Categorical variables were analyzed using Pearson χ2 tests, and continuous data were analyzed using t tests. We generated univariable and multivariable models to study the influence of HCM on outcomes, adjusting the model for relevant baseline characteristics. All analyses in our study were weighted using provided discharge weights to produce national estimates. Stata/IC software version 15.10 (StataCorp, LLC) was used for statistical analysis. Statistical significance was set at 2-tailed P < .05. Given the deidentified nature of the National Inpatient Sample data, our study was exempt from approval from the institutional review boards of Mount Sinai St Luke’s West and the Cleveland Clinic. This study was conducted as per the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline.
A total of 100 495 patients underwent TAVR during the study period. Of these, 230 patients (0.22%) had concomitant HCM. Compared with patients without HCM, those with HCM were more likely to be women (78.3% vs 46.7%; P < .001) and obese (28.3% vs 15.4%; P = .02) but less likely to have prior coronary artery bypass grafting (0.7% vs 21.4%; P = .01). Baseline demographic characteristics are presented in Table 1.
Patients with HCM had greater incidence of in-hospital mortality (18.6% vs 2.91% for non-HCM; adjusted odds ratio [aOR], 7.33; 95% CI, 3.26-16.44; P < .001), aortic dissection (2.33% vs 0.39%; aOR, 10.50; 95% CI, 2.53-43.53; P = .001), acute kidney injury (23.26% vs 12.24%; aOR, 2.62; 95% CI, 1.21-5.66; P = .01), and postoperative shock (16.28% vs 3.43%; aOR, 4.67; 95% CI, 1.97-11.05; P < .001) (Table 2). There were no differences in terms of vasopressor use, pacemaker requirement, vascular injury, major bleeding requiring transfusion, and respiratory failure between the 2 groups.
In this large, nationally representative study, we found that presence of HCM in patients undergoing TAVR was associated with markedly increased in-hospital mortality and complications. Current data on the association between HCM and postprocedural outcomes after TAVR are limited to small case reports and case series, which have described acute hemodynamic compromise after valve deployment.1-3 These cases highlight the difficulty in determining the contributions of each of the 2 obstructive lesions, and that provocable gradients might best be treated prior to TAVR to avoid the so-called suicide ventricle due to rapid removal of the afterload of aortic stenosis.1-3 The increased mortality observed in our study is likely attributable to unanticipated postprocedural hemodynamic compromise caused by unmasking of left ventricular outflow tract obstruction due to HCM, as previously reported.1,3 The higher rates of acute kidney injury may be associated with postprocedural hemodynamic alterations and volume depletion due to the use of diuretics to optimize volume status prior to TAVR. The increased use of vasoactive medications in the HCM cohort in our study was also described by others2; these may be needed to maintain afterload to counter the left ventricular outflow tract obstruction caused by HCM, as well as to treat the development of cardiogenic shock. The main limitations of our study were retrospective observational study design, a smaller number of patients in the HCM group, possibility of coding errors, and lack of granular information on hemodynamic data. Nevertheless, our results highlight a need for further work to investigate the impact of HCM, if any, on long-term outcomes following TAVR.
In this study, concomitant HCM was associated with substantially worse in-hospital outcomes, including cardiogenic shock, renal failure, and death, in patients undergoing TAVR.
Accepted for Publication: December 19, 2019.
Published: February 21, 2020. doi:10.1001/jamanetworkopen.2019.21669
Open Access: This is an open access article distributed under the terms of the CC-BY License. © 2020 Bandyopadhyay D et al. JAMA Network Open.
Corresponding Author: Ankur Kalra, MD, Regional Section of Interventional Cardiology at Cleveland Clinic Akron General, Cleveland Clinic Lerner College of Medicine, Department of Cardiovascular Medicine, Case Western Reserve University, 224 W Exchange St, Ste 225, Akron, OH 44302 (email@example.com).
Author Contributions: Drs Bandyopadhyay and Kalra had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Drs Bandyopadhyay, Chakraborty, Naidu, and Kalra contributed equally to the concept and design of the study.
Concept and design: Bandyopadhyay, Chakraborty, Amgai, Kapadia, Naidu, Kalra.
Acquisition, analysis, or interpretation of data: Chakraborty, Amgai, Braunwald, Naidu, Kalra.
Drafting of the manuscript: Bandyopadhyay, Chakraborty, Amgai, Naidu, Kalra.
Critical revision of the manuscript for important intellectual content: Amgai, Kapadia, Braunwald, Naidu, Kalra.
Statistical analysis: Bandyopadhyay, Chakraborty, Amgai, Naidu, Kalra.
Supervision: Chakraborty, Kapadia, Naidu, Kalra.
Conflict of Interest Disclosures: Dr Braunwald reported receiving grants from AstraZeneca, Daiichi Sankyo, Merck, and Novartis and personal fees from Amgen, Cardurion, MyoKardia, Novo Nordisk, and Verve outside the submitted work. No other disclosures were reported.
Additional Contributions: Muhammad Siyab Panhwar, MD (Tulane University, New Orleans, Louisiana), and Tanush Gupta, MD (Columbia University Medical Center, New York, New York), assisted in data analysis and Rishi Puri, MD (Cleveland Clinic, Cleveland, Ohio), provided editorial assistance. These individuals were not compensated for their contributions.
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