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Background: Cardiogenic shock (CS) associated with severe mitral regurgitation (MR) forebodes a high risk of morbidity and mortality. Transcatheter edge-to-edge repair (TEER) is a rapidly evolving technique for severe MR in haemodynamically stable patients. However, the safety and efficacy of TEER for severe MR in CS are not well established. Case summary: An 83-year-old male presented with dyspnoea and was hospitalized for heart failure. Chest X-ray revealed pulmonary oedema. Transthoracic echocardiography showed severely depressed ejection fraction (EF) with severe secondary MR. Right heart catheterization confirmed a low cardiac index. Diuretics and inotropes were administered. Due to persistent hypotension, we could not wean inotropes. The patient was deemed high risk for surgery by the heart team, and a decision was made to proceed with TEER with MitraClip. Under transoesophageal echocardiography and fluoroscopic guidance, two MitraClips were deployed sequentially. The MR grade was reduced to two mild jets subsequently. The patient was weaned off inotropes and eventually discharged. At the 30-day follow-up, he was participating in physical activities such as golf. Discussion: Cardiogenic shock complicated by severe MR carries high mortality. With severe MR, the forward stroke volume is lower than the stated EF leading to poor organ perfusion. Inotropes and/or mechanical circulatory support devices are paramount for initial stabilization; however, they do not treat underlying MR. Transcatheter edge-to-edge repair with MitraClip has been shown to improve survival in CS patients with severe MR in observational studies. However, prospective trials are lacking. Our case demonstrates the utility of MitraClip to treat severe secondary MR refractory to medical therapy in a CS patient. The heart team must evaluate risks and benefits of this therapy in CS patients.
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Although pulmonary function testing (PFT) is typically performed for heart transplant evaluation, the prognostic utility of PFTs after transplantation is unknown. We evaluated whether PFT parameters were correlated with outcomes following heart transplantation. METHODS: International Society for Heart and Lung Transplantation Thoracic Organ Transplant Registry data were utilized. Survival was assessed using Kaplan-Meier method and compared via log-rank test. Cox proportional hazard modeling was used to evaluate univariate and multivariate predictors of survival. RESULTS: Eight hundred two patients pretransplant PFT data were available for evaluation. Forced expiratory volume in 1 s (FEV1) < 50% predicted (P < 0.0001), and forced vital capacity (FVC) < 50% predicted each had significantly higher mortality (P = 0.001) compared with patients with FEV1 or FVC 50%-80% or >80%. FEV1/FVC < 0.7 was not associated with increased mortality. FEV1 and FVC below 50% both predicted longer lengths of stay (P = 0.028 for FEV1 and P = 0.0075 for FVC). After adjusting for male gender, age, body mass index, smoking history, chronic obstructive pulmonary disease, creatinine, albumin, and total bilirubin, FEV1 < 50% (hazard ratio, 4.91; P < 0.0001; 95% confidence interval, 2.69-8.94) and FVC < 50% (hazard ratio, 2.75; P = 0.003; 95% confidence interval, 1.4-5.4) both remained independent predictors of mortality. CONCLUSIONS: Abnormal pulmonary function (FEV1 or FVC below 50% of predicted) pre-heart transplantation is associated with increased mortality and longer lengths of stay posttransplant.
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Spontaneous coronary artery dissection is a serious and underreported clinical entity strongly associated with fibromuscular dysplasia (FMD). The female predominance of FMD may predispose many women to coronary artery dissection or other similar vascular pathologies. We present a case of a young woman who presented with a clinical tetrad of spontaneous coronary artery dissection, cardiogenic shock requiring extracorporeal membrane oxygenation, internal carotid dissections, and subacute cerebellar infarct secondary to underlying FMD. The patient's clinical course and vascular pathology are discussed. A review of the relevant literature of previously published similar cases, the incidence of spontaneous coronary artery dissection, and issues in the clinical management of spontaneous coronary artery dissection are also included.
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BACKGROUND: Sinus tachycardia (ST) is common after heart transplantation (HTx). The aim of the study was to evaluate the effect of diltiazem treatment during the first year after HTx on heart rate (HR), cardiac allograft function, and exercise capacity. METHODS: From the total cohort, 25 HTx recipients started diltiazem treatment 4±2 weeks after HTx and continued it for at least 1 year (diltiazem group). Each study case was matched to a control. All patients underwent hemodynamic assessment and cardiopulmonary exercise test (CPET) at 1 year after HTx. RESULTS: HR decreased in the diltiazem group from 99±11 bpm to 94±7 bpm (P=.03) and did not change in the controls (98±11 bpm vs 100±13 bpm, P=.14). The difference between the groups at 1 year after HTx was significant (P=.04). In the diltiazem group left ventricular (LV), stroke volume and ejection fraction increased (48±16 vs 55±17 mL, P=.02, and 60%±10% vs 62%±12% P=.03, respectively) but did not differ from controls. E/E' decreased (10.7±2.7 vs 7.3±1.9, P=.003) while cardiac index was higher (3.5±0.8 vs 3.1±0.5; P=.05) in the diltiazem group at 1-year follow-up. The absolute peak VO2 (21±4 vs 18±6 mL/kg/min; P=.05) and normalized peak VO2 (73%±17% vs 58%±14%; P=.004) were significantly higher in the diltiazem group. CONCLUSIONS: This study showed that diltiazem treatment reduces ST, may improve cardiac allograft function and exercise tolerance during the first year after HTx.