Aasim Afzal M.D.

Tecson, K. M., H. Hashemi, A. Afzal, T. A. Gong, P. Kale and P. A. McCullough (2019). “Community-Acquired Acute Kidney Injury as a Risk Factor of de novo Heart Failure Hospitalization.” Cardiorenal Med 9(4): 252-260.

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OBJECTIVES: Because patients with hospital-acquired acute kidney injury (AKI) are at risk for subsequent development of heart failure (HF) and little is known about the relation between community-acquired AKI (CA-AKI) and HF, we sought to determine if CA-AKI is a risk factor for incident HF hospitalization. METHODS: We utilized Baylor Scott & White Health databases at the primary care and inpatient hospitalization levels to identify adults without a prior history of HF who had 2 or more serum creatinine measurements within 13 months in the primary care setting. We defined CA-AKI as a serum creatinine increase >/=0.3 mg/dL or >/=1.5 times the baseline for consecutive values within a 13-month period. We created a flag for de novo HF hospitalization at 90, 180, and 365 days following CA-AKI evaluation. RESULTS: In the analyses, 210,895 unique adults were included, of whom 5,358 (2.5%) had CA-AKI. Those with CA-AKI had higher rates of comorbidities, higher rate of males (48 vs. 42%, p < 0.001), and were older (61.5 [50.3, 73.1] vs. 54.1 [42.8, 64.7] years, p < 0.001) than those who did not have CA-AKI. In total, 607 (0.3%), 833 (0.4%), and 1,089 (0.5%) individuals had an incident HF hospitalization in the 90, 180, and 365 days following the CA-AKI evaluation, respectively. After adjusting for demographic and clinical characteristics, patients with CA-AKI had >2 times the risk of de novo HF hospitalization compared with patients who did not have CA-AKI (90 days: 2.35 [1.83-3.02], p < 0.001; 180 days: 2.52 [2.04-3.13], p < 0.001; 365 days: 2.16 [1.77-2.64], p < 0.001). These multivariable models yielded strong predictive abilities, with the areas under the receiver-operating characteristic curve >0.90. CONCLUSION: After controlling for baseline and clinical characteristics, patients with CA-AKI were at approximately twofold the risk of de novo HF hospitalization (within 90, 180, and 365 days) compared with those who did not have CA-AKI. Hence, detecting CA-AKI may provide an opportunity for early intervention at the primary care level to possibly delay HF development.

Afzal, A., K. M. Tecson, A. K. Jamil, J. Felius, P. S. Garcha, S. A. Hall and S. A. Carey (2019). “The Effect of Obstructive Sleep Apnea on 3-Year Outcomes in Patients Who Underwent Orthotopic Heart Transplantation.” Am J Cardiol Apr 10. [Epub ahead of print].

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Despite the well-known association between obstructive sleep apnea (OSA) and cardiovascular disease, there is a paucity of data regarding OSA in orthotopic heart transplant (OHT) recipients and its effect on clinical outcomes. Hence, we sought to determine the association between OSA, as detected by polysomnography, and late graft dysfunction (LGD) after OHT. In this retrospective review of consecutive OHT recipients from 2012 to 2014 at our center, we examined LGD, i.e., graft failure >1 year after OHT, through competing risks analysis. Due to small sample size and event counts, as well as preliminary testing which revealed statistically similar demographics and outcomes, we pooled patients who had treated OSA with those who had no OSA. Of 146 patients, 29 (20%) had untreated OSA, i.e., OSA without use of continuous positive airway pressure therapy, at the time of transplantation. Patients with untreated OSA were significantly older, heavier, and more likely to have baseline hypertension than those with treated/no OSA. Although there were no differences between groups in regard to short-term complications of acute kidney injury, cardiac allograft vasculopathy, or primary graft dysfunction, there were significant differences in the occurrence of LGD. Those with untreated OSA were at 3 times the risk of developing LGD than those with treated/no OSA (hazard ratio 3.2; 95% confidence interval 1.3 to 7.9; p=0.01). Because OSA is a common co-morbidity of OHT patients and because patients with untreated OSA have an elevated risk of LGD, screening for and treating OSA should occur during the OHT selection period.

Kale, P. and A. Afzal (2018). “Stage B Heart Failure: To Strain or Not to Strain.” JACC Cardiovasc Imaging. May 11.[Epub ahead of print].

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Heart failure (HF) has been considered a progressive disorder than can be represented as a clinical continuum. In 2005, American College of Cardiology/American Heart Association updated the guidelines for management of HF and identified 4 states of heart failure with clinical recommendations for each stage. These guidelines helped address some of the confusion stemming from the symptom severity-based New York Heart Association functional classification. Symptom severity can change drastically over a short period either from medical therapy or absence of it, which can create confusion on treatment recommendations based solely on New York Heart Association functional classification. In the current schema, Stage B heart failure (SBHF) includes patients with Stage A HF who have structural heart disease but no current or prior symptoms of HF. It has been estimated that the number of patients in Stage B is about 2 times higher than Stages C and D combined. (Brief excerpt from this commentary, in press; no abstract available.)

Afzal, A., R. C. Vallabhan and P. A. McCullough (2017). “Acute kidney injury in cardiogenic shock: In search of early detection and clinical certainty.” Eur J Heart Fail: 1-3.

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This study stands out as the rst study to prospectively eval-uate AKI in patients with CS by KDIGO guidelines, based notonly on creatinine, but also on cystatin C.5The AKI mortal-ity results in this study are internally consistent as patients pre-senting with A KI had lower ejection fractions, higher Sequen-tial Organ Failure Assessment scores, and a higher incidenceof respiratory failure requiring mechanical ventilation.7Rates ofrenal replacement therapy were 14%, yet the 90-day mortalityrate was 38% suggesting that the majority of deaths in the rst20 days reected the natural history of CS treated with stan-dard of care in the cardiac catheterization laboratory and coro-nary care unit and were not amenable to ultraltration for pul-monary oedema/anuria or haemodialtration for hyperkalaemia orazotaemia.

Kopecky, K., A. Afzal, J. Felius, S. A. Hall, J. C. Mendez, M. Assar, D. P. Mason and A. S. Bindra (2017). “Bilateral sympathectomy for treatment of refractory ventricular tachycardia.” Pacing Clin Electrophysiol: 2017 Aug [Epub ahead of print].

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Ventricular tachycardia (VT) commonly occurs in patients with ischemic or non-ischemic cardiomyopathy and requires anti-arrhythmic drugs, ablation or advanced circulatory support. However, life-threatening VT may be refractory to these therapies, and may cause frequent implantable cardioverter defibrillator (ICD) discharges. Left cardiac sympathetic denervation reduces the occurrence of these fatal arrhythmias by inhibiting the sympathetic outflow to the cardiac tissue. We present a 69-year-old man with non-ischemic cardiomyopathy, life-threatening VT, and hemodynamic instability with numerous ICD discharges who remained refractory to antiarrhythmic drug therapy and ablation attempts. He was effectively treated with bilateral cardiac sympathectomy. Six months later, he remained free of VT with no ICD discharges.