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A Heart of Stone
S60 Journal of Cardiac Failure Vol. 23 No. 8S August 2017 hyperparathyroidism causing myocardial calcification appears to be irreversible and can lead to graft failure- an important consideration for transplant patients.
Table 1. Variable Age at implant, years Sex, women Black race BMI at implant Hypertension Diabetes mellitus Ischemic etiology Creatinine, mg/dl BUN, mg/dl Device type: HMII HVAD Intention of Implant: Bridge to decision Bridge to transplant Destination therapy
Mean ± SD or N (%frequency) 55 ± 12 70 (26%) 182 (68%) 29 ± 6 173 (65%) 101 (38%) 90 (34%) 1.31 ± 0.6 24 ± 15 110 (41%) 156 (59%) 32 (12%) 139 (52%) 95 (36%)
159 A Heart of Stone Abhishek Dutta, Aysha Amjad, Hanumantha Jogu, Geoffrey Te Jao; Wake Forest University, Winston Salem, North Carolina Myocardial calcification is rare. It can be broadly dystrophic, metastatic, or idiopathic. We describe a case of myocardial calcification due to endstage renal disease from uncontrolled tertiary hyperparathyroidism. Description: A 27 year old AfricanAmerican male with end-stage renal disease (ESRD) on hemodialysis, tertiary hyperparathyroidism s/p subtotal parathyroidectomy, and uncontrolled hypertension, presented to the cardiology clinic as a referral from his nephrologist to further evaluate progressively worsening dyspnea .The patient had a history of focal segmental glomerulosclerosis with two failed cadaveric renal transplants. He had high serum calcium and PTH level for a prolonged time following his second renal transplant .The patient’s graft function failed from tertiary hyperparathyroidism and he is on hemodialysis thrice weekly for last three years.The patient first started having exertional dyspnea six months ago,limiting his ability to perform daily activities. He slept on two pillows, but denied PND. He denied any other cardiac symptoms. He was admitted to the hospital a month ago for worsening dyspnea. The impression then, was volume overload secondary to missed hemodialysis sessions.CT chest and abdomen done during admission showed a diffuse calcification of the left ventricle, mitral valve, and a small pericardial effusion .There was no evidence of pulmonary granulomatous lesions, malignancy, calcification of other major organs. Nuclear stress test showed no inducible ischemia . AFB, fungal cultures and CMV titres were negative.The patient was hypertensive during his clinic visit. EKG showed sinus rhythm, with left ventricular hypertrophy (LVH). .TTE showed a concentric LVH with prominent hyperechoic myocardium with an EF of 50%Discussion : Myocardial calcification is rare. It can occur by two mechanisms: dystrophic or metastatic. Dystrophic calcification occurs in dead and damaged tissues with normal calcium and phosphate balance. Metastatic calcification occurs with derangement of calcium and phosphorus metabolism.Metastatic calcification is rarely isolated to single organ but not the case for our patient.Fairly exhaustive investigations to rule out other etiologies were unrevealing. Infectious causes were ruled out. We believe that the myocardial calcification in our patient can be explained by the altered calcium and phosphate metabolism with tertiary hyperparathyroidism . His persistently elevated calcium-phosphorus product despite subtotal parathyroidectomy is a continuing risk factor. Uncontrolled tertiary
160 A Retrospective Review of Sacubitril-Valsartan Combination Use in a Diverse Advanced Heart Failure Patient Population in a Community Hospital Tamra Ward; Total Heart Center at Memorial Regional Hospital, Hollywood, Florida Introduction: Sacubitril/valsartan combination (SVC) is a new member of the armamentarium for the treatment of heart failure (HF). In the PARADIGM-HF trial, when compared to enalapril, SVC showed a 21% reduction in the composite endpoint of death from cardiovascular causes or hospitalization for HF in mostly NYHA function class (FC) II to III HF with reduced ejection fraction (HFrEF). After its FDA approval in 2015, SVC received a Class I recommendation from the 2016 focused ACC/AHA/ HFSA guidelines for patients with chronic HFrEF to reduce morbidity and mortality. These guidelines also recommended replacement with SVC for patients with chronic symptomatic HFrEF NYHA Class II or III who tolerate an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB). Since the publication of these guidelines, the usage of SVC has increased in our institution. On average $2000 per day is spent on the treatment of each of our HF patients. Interestingly, in contrast to the patient demographic in the PARADIGM-HF trial, we have used SVC in a large percentage of African American (46.67% vs. 5.1%) and/or NYHA FC IV (40% vs. 0.8%) patients. The purpose of this study was to describe our experience of SVC use in a diverse advanced HF patient population. Methods: A retrospective chart review was conducted among adult advanced HF patients who had SVC initiated during hospitalization from March 26, to October 30, 2016. Adherence to FDA-approved indications for use, appropriateness of dosing, adverse events, 30-day readmission rates, and cardiovascular death were evaluated. Descriptive statistics were used to analyze the data. Results: Using our electronic chart database, a total of 30 advanced HF patients were identified during and 60% (n = 18) were discharged on SVC. The characteristics of this cohort included mean age of 57 years, male 80%, African Americans 47%, systolic HF 77%, NYHA FC III/IV 90%, and mean ejection fraction 22%. Of these, one patient was readmitted within 30 days for HF exacerbation. Patients who experienced an adverse event were 63%, with 31.5% requiring discontinuation of therapy (4 due to hypotension and 2 due to acute kidney injury). SVC was discontinued in an additional 6 patients due to cost. Twenty-five (83.3%) patients were initiated on the correct starting dose of SVC per manufacturer-recommended dosing. Although the manufacturer suggests a 36-hour washout period before the administration of SVC in patients who were previously on an ACEI, this occurred in only 10 of the 12 (83.3%) patients who were previously on an ACEI. One (3.3%) patient experienced angioedema but did not occur during the washout period. Lastly, 2 SVC unrelated cardiovascular deaths were reported. Conclusion: SVC is used in a broad adult advanced HF population within our institution. Despite the small sample size, the risk reduction provided by SVC is expected to have a substantial impact on the care of these patients, including those who were not largely represented in the trial that brought SVC to market.
Table 1. Variable Age at implant, years Sex, women Black race BMI at implant Hypertension Diabetes mellitus Ischemic etiology Creatinine, mg/dl BUN, mg/dl Device type: HMII HVAD Intention of Implant: Bridge to decision Bridge to transplant Destination therapy
Mean ± SD or N (%frequency) 55 ± 12 70 (26%) 182 (68%) 29 ± 6 173 (65%) 101 (38%) 90 (34%) 1.31 ± 0.6 24 ± 15 110 (41%) 156 (59%) 32 (12%) 139 (52%) 95 (36%)
159 A Heart of Stone Abhishek Dutta, Aysha Amjad, Hanumantha Jogu, Geoffrey Te Jao; Wake Forest University, Winston Salem, North Carolina Myocardial calcification is rare. It can be broadly dystrophic, metastatic, or idiopathic. We describe a case of myocardial calcification due to endstage renal disease from uncontrolled tertiary hyperparathyroidism. Description: A 27 year old AfricanAmerican male with end-stage renal disease (ESRD) on hemodialysis, tertiary hyperparathyroidism s/p subtotal parathyroidectomy, and uncontrolled hypertension, presented to the cardiology clinic as a referral from his nephrologist to further evaluate progressively worsening dyspnea .The patient had a history of focal segmental glomerulosclerosis with two failed cadaveric renal transplants. He had high serum calcium and PTH level for a prolonged time following his second renal transplant .The patient’s graft function failed from tertiary hyperparathyroidism and he is on hemodialysis thrice weekly for last three years.The patient first started having exertional dyspnea six months ago,limiting his ability to perform daily activities. He slept on two pillows, but denied PND. He denied any other cardiac symptoms. He was admitted to the hospital a month ago for worsening dyspnea. The impression then, was volume overload secondary to missed hemodialysis sessions.CT chest and abdomen done during admission showed a diffuse calcification of the left ventricle, mitral valve, and a small pericardial effusion .There was no evidence of pulmonary granulomatous lesions, malignancy, calcification of other major organs. Nuclear stress test showed no inducible ischemia . AFB, fungal cultures and CMV titres were negative.The patient was hypertensive during his clinic visit. EKG showed sinus rhythm, with left ventricular hypertrophy (LVH). .TTE showed a concentric LVH with prominent hyperechoic myocardium with an EF of 50%Discussion : Myocardial calcification is rare. It can occur by two mechanisms: dystrophic or metastatic. Dystrophic calcification occurs in dead and damaged tissues with normal calcium and phosphate balance. Metastatic calcification occurs with derangement of calcium and phosphorus metabolism.Metastatic calcification is rarely isolated to single organ but not the case for our patient.Fairly exhaustive investigations to rule out other etiologies were unrevealing. Infectious causes were ruled out. We believe that the myocardial calcification in our patient can be explained by the altered calcium and phosphate metabolism with tertiary hyperparathyroidism . His persistently elevated calcium-phosphorus product despite subtotal parathyroidectomy is a continuing risk factor. Uncontrolled tertiary
160 A Retrospective Review of Sacubitril-Valsartan Combination Use in a Diverse Advanced Heart Failure Patient Population in a Community Hospital Tamra Ward; Total Heart Center at Memorial Regional Hospital, Hollywood, Florida Introduction: Sacubitril/valsartan combination (SVC) is a new member of the armamentarium for the treatment of heart failure (HF). In the PARADIGM-HF trial, when compared to enalapril, SVC showed a 21% reduction in the composite endpoint of death from cardiovascular causes or hospitalization for HF in mostly NYHA function class (FC) II to III HF with reduced ejection fraction (HFrEF). After its FDA approval in 2015, SVC received a Class I recommendation from the 2016 focused ACC/AHA/ HFSA guidelines for patients with chronic HFrEF to reduce morbidity and mortality. These guidelines also recommended replacement with SVC for patients with chronic symptomatic HFrEF NYHA Class II or III who tolerate an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB). Since the publication of these guidelines, the usage of SVC has increased in our institution. On average $2000 per day is spent on the treatment of each of our HF patients. Interestingly, in contrast to the patient demographic in the PARADIGM-HF trial, we have used SVC in a large percentage of African American (46.67% vs. 5.1%) and/or NYHA FC IV (40% vs. 0.8%) patients. The purpose of this study was to describe our experience of SVC use in a diverse advanced HF patient population. Methods: A retrospective chart review was conducted among adult advanced HF patients who had SVC initiated during hospitalization from March 26, to October 30, 2016. Adherence to FDA-approved indications for use, appropriateness of dosing, adverse events, 30-day readmission rates, and cardiovascular death were evaluated. Descriptive statistics were used to analyze the data. Results: Using our electronic chart database, a total of 30 advanced HF patients were identified during and 60% (n = 18) were discharged on SVC. The characteristics of this cohort included mean age of 57 years, male 80%, African Americans 47%, systolic HF 77%, NYHA FC III/IV 90%, and mean ejection fraction 22%. Of these, one patient was readmitted within 30 days for HF exacerbation. Patients who experienced an adverse event were 63%, with 31.5% requiring discontinuation of therapy (4 due to hypotension and 2 due to acute kidney injury). SVC was discontinued in an additional 6 patients due to cost. Twenty-five (83.3%) patients were initiated on the correct starting dose of SVC per manufacturer-recommended dosing. Although the manufacturer suggests a 36-hour washout period before the administration of SVC in patients who were previously on an ACEI, this occurred in only 10 of the 12 (83.3%) patients who were previously on an ACEI. One (3.3%) patient experienced angioedema but did not occur during the washout period. Lastly, 2 SVC unrelated cardiovascular deaths were reported. Conclusion: SVC is used in a broad adult advanced HF population within our institution. Despite the small sample size, the risk reduction provided by SVC is expected to have a substantial impact on the care of these patients, including those who were not largely represented in the trial that brought SVC to market.