Correlation Between Aortic Angulation and Outcomes of Transcatheter Aortic Valve Replacement With New-Generation Valves.

The aim of this study was to assess the correlation of aortic angulation (AA) on immediate postprocedural and long-term outcomes following transcatheter aortic valve replacement (TAVR) with new-generation valves. There is limited and conflicting data on the impact of AA on short- and long-term outcomes in patients undergoing TAVR. Available studies to date were done with first-generation valves. We assessed 179 patients who underwent TAVR with either a balloon-expandable or self-expandable valve at our institute from May 2014 to June 2017 and had multislice computed tomography scans available for AA evaluation. All included patients received a second- or third-generation valve. TAVR endpoints, device success, and adverse events were defined according to the Valve Academic Research Consortium-2 criteria. The mean AA of the study population was 49.05 ± 10.07. Patients were divided into 2 groups: AA <49 and AA ≥49, and then further subdivided by valve type. There were no difference in mean age, The Society for Thoracic Surgery (STS) score, or race distribution between the AA <49 and AA ≥49 groups. The preimplantation balloon valvuloplasty rate was higher in patients with AA ≥ 49 compared to patients with AA <49, (70% vs 55.1%, P = 0.04). There was no difference in re-hospitalization, pacemaker implantation, postprocedural aortic regurgitation or mortality between patients with AA <49 and AA ≥49 irrespective of valve type (P < 0.05). AA does not significantly affect short- or long-term outcomes in patients who undergo TAVR with new-generation balloon-expandable or self-expandable valves.

An unusual cause of transient ischemic attack in a patient with pacemaker.

Pacemaker lead malposition in various locations has been described in the literature. Lead malposition in left ventricle is a rare and an underdiagnosed complication. We present a 77-year-old man with history of atrial fibrillation and pacemaker placement who was admitted for transient ischemic attack. He was on aspirin, beta blocker, and warfarin with subtherapeutic international normalized ratio. His paced electrocardiogram showed right bundle-branch block, rather than the typical pattern of left bundle-branch block, suggesting pacemaker lead malposition. Further, his chest X-ray and echocardiogram confirmed the pacemaker lead position in the left ventricle instead of right ventricle. He refused surgical removal of the lead and we increased his warfarin dose. Diagnosis of lead malposition in left ventricle, though easy to identify in echocardiogram, requires high index of clinical suspicion. In asymptomatic patients, surgical removal may be deferred for treatment with lifelong anticoagulation.

Causes and consequences of systemic venous hypertension.

The causes of systemic venous hypertension (SVHT) include cardiac- and circulatory-related factors, whereas its consequences include the congestion of hepatic, splanchnic, and peripheral circulations, which contribute significantly to the clinical congestive heart failure syndrome. Based on a disequilibrium in hydrostatic and oncotic pressures, the increased filtration and formation of interstitial fluid at these sites with an accompanying increase in lymph flow mandates an increment in lymphatic drainage to protect against such congestion and the appearance of edema and ascites. However, lymph flow via the thoracic duct into systemic veins is opposed by elevations in central venous pressure. Various management strategies have the potential to prevent and/or correct SVHT. The case of a 54-year-old man with a dilated cardiomyopathy who presented with decompensated biventricular failure, expressed as anasarca and ascites, is used to illustrate the importance of SVHT.

Elevated serum cobalamin in patients with decompensated biventricular failure.

BACKGROUND: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. METHODS AND RESULTS: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 +/- 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 +/- 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. CONCLUSIONS: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.