Idioventricular Rhythm: A Rare Presentation of Left Ventricular Pseudoaneurysm Following Radiofrequency Ablation.

Left ventricular pseudoaneurysm (PsA) is a rare complication of radiofrequency ablation (RFA) of cardiac arrhythmias. Presentation can vary widely in terms of timeline, signs, and symptoms. Idioventricular rhythm is a rare presentation of PsA post-ablation. No cases of post-ablation PsA presenting with idioventricular rhythm have been reported in the literature to date. A 72-year-old male presented with symptomatic idioventricular rhythm 34 days post RFA for premature ventricular complexes (PVCs). A PsA involving the distal anterolateral of his left ventricle wall was identified on transthoracic echo and computed tomography (CT). This patient underwent surgical patch repair which resolved his ventricular arrhythmia.

Posttransplant atrial fibrillation: Evidence of early posttransplant recipient-to-donor atrioatrial connections.

INTRODUCTION: Atrial fibrillation and atrial flutter originating from the donor s heart is a commonly reported complication post heart transplant. Atrial tachyarrhythmia originating from the recipient s heart, propagated through recipient-to-donor connections, is rare with only few cases reported in the literature; most reported cases from our review occur years post-transplant. CASE: A 47-year-old male presented with atrial tachycardia 6 months post heart transplant. Electrophysiologic study demonstrated atrial fibrillation originating from native heart and propagated through atrio-atrial connections to the donor heart. This arrhythmia was successfully terminated with radiofrequency ablation. CONCLUSION: Atrio-atrial connection between recipient and donor can form as early as a few months post heart transplant. Radiofrequency ablation appears to be an effective treatment for atrial fibrillation propagated through donor-to-recipient connections.

Association of Maximum Troponin Levels With Diagnosis of Acute Myocardial Infarction and Elevated Risk of Mortality.

Background: Cardiac troponins I and T are highly sensitive and specific markers for acute myocardial infarction (AMI). However, a wide range of non-AMI conditions can also cause significant elevations in cardiac troponins. Given the deleterious impact of misdiagnosis of AMI, the ability to risk-stratify patients who present with an elevated troponin is paramount. We hypothesized that the maximum troponin level would be more predictive of mortality and the diagnosis of AMI than the initial troponin level or change in troponin level. Methods: Patient records from a 9-hospital system (n=30,173) in Texas were reviewed during a 24-month period in 2016-2017. Data collected for patients aged ≥40 years included International Classification of Diseases, Tenth Revision diagnoses, troponin I, demographic data (age, sex, smoking history, and chronic medical conditions), and death during hospitalization. We used logistic regression with the Firth penalized likelihood approach to determine the predictive ability of initial, maximum, and change in troponin level for mortality and the diagnosis of AMI. Results: Demographic characteristics of our cohort included a median age of 70 years, with 48.05% male and 51.95% female. The most common preexisting risk factor was hypertension in 78.81% of the cohort. Notable findings from the logistic regression include the predictive ability of maximum troponin on the odds of death by 0.7% for each unit of increase in troponin value. Also, the odds of AMI increased by 3.1% for each unit of increase in the maximum troponin value. Conclusion: Regardless of the level, a detectable amount of troponin in the serum results in a significantly elevated risk of mortality. Many patients with elevated troponin levels leave the hospital without a specific diagnosis, which can lead to poor outcomes because a detectable troponin does not represent a no-risk population. Our study demonstrates that maximum troponin level is a more sensitive and specific predictor of mortality than initial or change in troponin. Similarly, maximum troponin is the most predictive of AMI vs other causes of troponin elevation, likely because of the correlation between rising troponin levels and cardiomyocyte damage. Further studies are needed to correlate maximum troponin levels and clinical manifestations, which may be helpful in redefining AMI so that AMI can be distinguished more easily from non-AMI diagnoses.

Page Kidney From a Subcapsular Urinoma Following Contralateral Radical Nephrectomy.

Page kidney is a rare cause of hypertension and kidney injury; it results from extrinsic compression of the kidney due to fluid accumulation in the subcapsular space. Hypertensive crisis may be the only presenting clinical sign in patients with Page kidney. Urinomas are a very rare cause of Page kidney with very few cases reported in the literature. Urinoma should be suspected in patients presenting in hypertensive crisis who have a history of recent abdominal trauma, genitourinary malignancy, and renal instrumentation. Patients diagnosed with Page kidney from a urinoma should be managed with the least invasive means possible.

Relapsing Multiple Myeloma Presenting as Cardiac Tamponade and Obstructive Uropathy.

Cardiac tamponade is a rare manifestation of relapsing extramedullary multiple myeloma and portends poor prognosis. No cases of cardiac tamponade with co-occurring renal obstruction from plasmacytoma have been reported in the literature, making this case a unique presentation of relapsing multiple myeloma. The presence of known malignancy should not limit our differential diagnosis when evaluating patients with signs of cardiac tamponade.