Case Report
Herein we describe a case report of a low body weight 74-year old male patient who presented with acute decompensated heart failure (HF) with both end-stage systolic and diastolic HF including right ventricular (RV) failure.
He is previously known to have type II Diabetes Mellitus (DM), Hypertension and previous presumed diagnosis of Dilated Cardiomyopathy (DCM) in another facility on non-optimal medical therapy (OMT) for the past two years.
On presentation patient was orthopneic and in dyspnea NYHA functional class IV over the past 10 days.
Initial work up was done. 2D echo showed severe LV dysfunction, with estimated LV ejection fraction (EF) of 15-20% (Video_1), with global hypokinesia and akinesia of apex, inferior and lateral wall and a picture of ischemic dilated cardiomyopathy (IDCM) with severe RV dysfunction demonstrating interventricular septal flattening more during diastole due to RV volume overload (Video_2, Figure_1) with associated severe pulmonary hypertension (PH) and an estimated systolic pulmonary artery pressure (PAPs) of 80 mm Hg (Figure­_2). There was grade IV severe MR (Video_3 & 4, Figure_3 & 4) and torrentially significant tricuspid regurgitation (TR) (Video_5 & 6, Figure_5 & 6) with illustrated hepatic vein systolic flow reversal on Pulsed wave doppler (PWD) (Figure_7, Video_7).
Restrictive pattern grade III diastolic dysfunction with elevated LV filling pressure by Tissue doppler imaging (TDI) was noted (Figure_8 & 9).
Lung ultrasound (LUS) demonstrated frequent B-lines on both lungs (Video_8) denoting pulmonary interstitial edema and volume overload.
The patient was admitted in the coronary care unit (CCU) and started on Frusemide infusion after an IV bolus dose of 40mg, besides Spironolactone, Ramipril, Rosuvastatin, Empagliflozin and Aspirin.
Patient had sinus rhythm on Electrocardiogram (ECG) with Interventricular conduction delay and a duration of QRS complex ≥ 125 ms (Figure_10).
Chest X-Ray showed signs of pulmonary congestion (Figure_11).
N-terminal pro B-type natriuretic peptide (NT-proBNP) was over 9,000 pg/ml. Serum potassium 3.8 mmol/L, serum sodium 141 mmol/L, Hemoglobin 14 gm/dl, serum Creatinine 107 Umol/L and calculated creatinine clearance of 45 ml/min.
Patient improved on medical therapy. And then on day four during admission coronary angiography (CAG) was done and revealed triple vessel disease with significant 90% long diffuse tight lesions in proximal to mid left anterior descending (LAD) artery, critical 90% lesion in both obtuse marginal (OM) branches of left circumflex (LCX) artery and chronic total occlusion (CTO) of right coronary artery (RCA) with retrograde filling from LAD and LCX arteries (Video_9 & 10).
In view of severe grade IV MR, triple vessel disease and severe LV and RV dysfunction; we recommended coronary artery bypass graft surgery (CABG) combined with mitral valve repair (MVr), then followed by implantation of a cardiac resynchronization therapy defibrillator (CRT-D) device if no LV function improvement observed after coronary revascularization plus OMT.
Patient had a QRSd ≥ 125 ms on ECG, and hence is a good candidate for a CRT-D device therapy after coronary revascularization in case LV dysfunction persisted.
While waiting for myocardial viability stress test to be done before revascularization and with efforts to improve LV function, we started maximally tolerated doses of different ACEI and ARBs including Enalapril, Ramipril and Valsartan, as well as Beta-blockers including Nebivolol, Metoprolol and Carvedilol. This is in addition to Mineralocorticoid receptor antagonists (MRA) and sodium-glucose cotransporter-2 (SGLT-2) inhibitors, aspirin and high doses of loop diuretics.
Patient could not afford Sacubitril/Valsartan due to cost burden.
He experienced recurrent hospitalization due to acute decompensated heart failure. After hospital discharge, he showed up every other day in hospital for Furosemide injection to alleviate his HF symptoms. Patient was in Dyspnea NYHA class IV with symptoms at rest and significant orthopnea and PND with dramatic impairment of his life quality.
Three weeks later during repeated CCU admission Sacubitril/Valsartan was offered to the patient after we ensured a 36-hour washout period which is required when switching from ACEI to Sacubitril/Valsartan. Started on a dose of 24mg/26mg PO BID.
We observed a dramatic improvement in symptoms from NYHA class IV to NYHA class II that occurred 5 days only after starting Sacubitril/Valsartan during CCU setting. Then further improvement to NYHA class I occurred after 2 weeks of treatment.
After discharge from hospital patient was walking 4 kilometers daily with exceptionally good effort tolerance and no symptoms. He stopped showing up in the hospital for Furosemide injections.
In addition, there was a major favorable change in his quality of life.
NT-proBNP reduced from above 9,000 pg/ml on admission to 800 pg/ml after two weeks.
Screening 2D echo on hospital discharge showed dramatic improvement of LV function. LV EF improved from 15-20% to 40-45% with significant reversal of LV remodeling (Video_11, Figure_12).
MR severity improved from grade IV to grade II (Video_12 & 13, Figure_13), and severe TR improved to mild grade I (Video_14, Figure_14) with no hepatic vein systolic flow reversal on PWD. In addition, PAPs fell from 80 mm Hg to normal value of 30 mm Hg (Figure_15).
The patient’s diastolic function improved from grade III to grade I with normal LV filling pressure (Figure_16).
Sacubitril/Valsartan dose then increased to 49 mg/51 mg PO BID
Three weeks later, myocardial perfusion scintigraphy using nitrate-augmented 99mTc-Sestamibi showed evidence of viable myocardial perfusion of the LAD and LCX/OM territories. However, there was non-viable myocardial perfusion in the RCA territory.
Due to the fact that our patient showed improvement of myocardial function and dramatic reduction of MR severity after treatment with Sacubitril/Valsartan, we found that revascularization by percutaneous coronary intervention (PCI) is a more convenient option for the fragile low body weight elderly patient with a much lower overall operative risk than that of surgery, and in addition that he will no longer need MVr for secondary MR.
Elective PCI done successfully to LAD and LCX/OM arteries with no peri-operative events (Video_15 & 16).
The patient showed further improvement of LV function post PCI. LV EF improved from 35-40% to 50% on follow up 2D echo (Video 17). He was completely asymptomatic and with particularly good effort tolerance.
The patient maintained preserved LV EF on follow up for 18 months later while on Sacubitril/Valsartan.