Faculty Bibliography

PURPOSE: Heart transplantation from Hepatitis C (HCV) viremic donors is becoming increasingly used due to advent of direct acting antiviral drugs with almost 100% cure. There are limited data about its impact on cardiac allograft vasculopathy (CAV). We report the incidence of CAV in heart transplant recipients from HCV viremic donors (nucleic amplification test positive; NAT+) compared to non-HCV infected donors (NAT-).
METHOD(S): We retrospectively reviewed coronary angiograms with intravascular ultrasound (IVUS) of heart transplant recipients at our institution from January 5, 2018 to September 17, 2019. The presence of CAV was graded according to ISHLT guidelines. IVUS was performed as per our lab protocol on the left main and left anterior descending arteries. Maximal intimal thickness (MIT) was measured with advanced quantification software as per protocol. MIT >= 5mm was considered significant for future adverse outcomes.
RESULT(S): LHC and IVUS was performed on 24 heart transplant recipients (mean age 56; 70% male) at 1- year post transplant. Eleven of these patients were transplanted from NAT+ donors. Thirteen patients received a NAT- donor heart. Two recipients (18.7%) of NAT+ donors had CAV grade >= 1 compared to 2 (16.7%) from NAT- donors (p=1). MIT >= 5mm was seen in 88.9% of NAT+ vs 50% of NAT- recipients (p=0.14) (Figure). The mean MIT was 76mm and 65mm for NAT+ and NAT- group, respectively. Both NAT+ and NAT- donor recipients exhibit mostly eccentric (84.2%) and few (15.7%) demonstrated concentric plaques. There was no heterogeneity in the data after adjusting for risk factors for CAD and donor LHC.
CONCLUSION(S): Our data show no difference in the presence of (CAV >= grade 1) or subclinical atherosclerosis at 1 year among NAT+ donor recipients. HCV viremia is a known risk factor for accelerated atherosclerosis and the consequence of prolonged donor viremia on the recipient is not known. A larger cohort and further longitudinal follow-up is needed to assess the validity of this trend and its prognostic implications.
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Background Arrhythmogenic cardiomyopathy (ACM) can mimic inflammatory processes. We present a complex patient with scleroderma (Sc)-dermatomyositis overlap syndrome (Sc-DM) and cardiac disease. Case A 57-year-old woman with family history of Sc presented with progressive weakness, dyspnea, edema, and Raynaud's (1A). Troponin was 1.6 ng/mL and CRP was 13.2 mg/L. EKGs revealed sinus rhythm with RBBB and AV sequential pacing with multifocal PVCs (1B-C). CT chest showed bibasilar fibrosis (1D). Echocardiography revealed biventricular dysfunction. Cardiac catheterization showed non-obstructive coronaries and a cardiac index of 1.8 L/min/m2. Cardiac MRI had diffuse biventricular subendocardial late gadolinium enhancement (1E). Electromyography revealed proximal myopathy. Rheumatologic workup was consistent with seronegative Sc-DM. Decision-making She was treated with steroids, mycophenolate, IV immunoglobulins, diuretics, and inotropes. Her course was complicated by recurrent VT cardiac arrests, prompting escalation to VA-ECMO. She underwent cardiac transplant on day 9 of ECMO. Pathology revealed biventricular fibrofatty replacement consistent with ACM (1F-G), patchy fibrosis of the pericardium, and mitral valve with thickened and fused chordae suggestive of inflammatory changes from Sc (1H-I). Conclusion This case highlights an atypical presentation of ACM in a patient with Sc-DM and the multidisciplinary approach necessary for proper diagnosis and management. [Figure presented]
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Aortic valve intervention (AVI) in patients with a severe aortic stenosis (AS) and a preserved left ventricular ejection fraction (LVEF) is controversial. Mitral annular plane systolic excursion (MAPSE) is an easily acquired metric of left ventricular longitudinal shortening. We sought to investigate if an asymptomatic decrease in MAPSE preceded the need for AVI in asymptomatic patients with AS and a preserved LVEF. In this retrospective cohort study, we identified 205 consecutive patients (56% male, 73 ± 11 years) with at least a moderate AS and a normal LVEF who underwent a serial outpatient transthoracic echocardiography (TTE) from 2006 to 2013. Apical TTE images were reviewed and (the average of septal, lateral, anterior, and inferior) MAPSE was measured. We examined the association of change in MAPSE with aortic valve area and LVEF over time and used time-varying Cox models to examine the risk of AVI. MAPSE correlated with aortic valve area (Spearman r = 0.18, p = 0.02) and decreased with subsequent TTE, whereas LVEF was "maintained." For each 1-mm reduction in MAPSE, the age- and gender-adjusted hazard ratio (HR) for AVI was 1.15 (95% confidence interval [CI] 1.01 to 1.31, p = 0.04). A MAPSE decrease of >2 mm/TTE was significantly associated with an increased risk of AVI, with an adjusted HR of 1.95 (95% CI 1.04 to 3.66, p = 0.04), whereas a MAPSE decrease of >1.5 mm/year trended toward an association with an increased risk of AVI (HR 1.61, 95% CI 0.95 to 2.74, p = 0.08). In conclusion, in asymptomatic patients with at least a moderate AS and a preserved LVEF, an asymptomatic decrease in MAPSE was associated with the clinical need for AVI despite ongoing preservation of LVEF.

Implantable cardioverter-defibrillator (ICD) implantation outside practice guidelines remains contentious, particularly during the mandated waiting periods in patients with recent cardiac events. We assessed the prevalence and outcomes of non-guideline-based (NGB) ICD implantations in a tertiary academic medical center, with a specific focus on adjudication of arrhythmia events. All patients who underwent initial primary prevention ICD implantation at our institution from 2004 to 2012 were categorized as having received guideline-based (GB) or NGB implants and were retrospectively assessed for first episode of appropriate ICD therapy and total mortality. Of 807 patients, 137 (17.0%) received NGB implants. During a median follow-up of 2.9 years, patients with NGB implants had similar times to first appropriate ICD therapy (median time to event 1.94 vs 2.17 years in patients with GB implants, p = 0.20). After multivariable analysis, patients with NGB implants remained at higher risk for death (hazard ratio 1.54, 95% confidence interval 1.1 to 2.2, p = 0.03) but not appropriate ICD therapy (hazard ratio 0.83, 95% confidence interval 0.5 to 1.3, p = 0.51). Furthermore, only 1 of 125 patients who underwent implant within the 40-day waiting period after myocardial infarction or 3-month waiting period after revascularization or cardiomyopathy diagnosis received an appropriate therapy within this period. In conclusion, few patients received NGB ICD implants in our academic medical center. Although these patients have similar long-term risk of receiving appropriate ICD therapy compared with patients with GB implants, this risk is very low during the waiting periods mandated by clinical practice guidelines. These results suggest that there is little need to rush into implanting ICDs during these waiting periods.

Guidelines recommend aggressive goals for lipid and blood pressure reduction for high risk patients with diabetes mellitus and atherosclerotic coronary disease. However, it remains unclear how many patients achieve treatment goals versus the number of people merely placed on treatment. We conducted an observational study in an academic cardiology clinic. A total of 926 patients with atherosclerotic cardiovascular disease and concomitant diabetes mellitus met criteria. Mean age was 68.4 ± 10.2, 65.6% were male, and 86.8% were Caucasian. By the last visit a high percentage of patients were receiving recommended medications. Mean LDL-cholesterol achieved was 80.4 mg/dl with 40.9% reaching ≤ 70 mg/dl, and 61.7% reaching SBP ≤ 130 mmHg. Many patients with diabetes mellitus and atherosclerotic cardiovascular disease are prescribed recommended medications; however, few achieve guidelines-specified therapeutic goals for LDL-cholesterol and blood pressure. Studies evaluating performance improvement should include percentage of patients reaching treatment goals. Mechanisms underlying the treatment gap need to be identified and addressed.