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Toxoplasma encephalitis (TE) is usually diagnosed in advanced stages of HIV infection when the CD4+ count is <100-200 cells/µl. A 55-year-old woman with HIV/AIDS, well controlled on antiretroviral therapy (ART), CD4+ count in the 300 cells/μl range for >1 year presented with acute onset of headache, nausea and vomiting. She had been on her current ART regimen consisting of raltegravir, co-formulated emtricitabine/tenofovir and etravirine for three years and had been off Pneumocystis prophylaxis for 10 months (trimethoprim-sulfamethoxazole). Brain MRI showed multiple ring-enhancing, supratentorial and infra-tentorial parenchymal lesions suspicious for metastases. She had no other evidence of metastatic disease in her body. The possibilities of TE and primary CNS lymphoma were considered but deemed unlikely given the high CD4+ count. A brain biopsy demonstrated Toxoplasma tachyzoites. There was no evidence of lymphoma or carcinoma. Anti-toxoplasma treatment yielded good initial clinical and radiographic responses. While on TE maintenance therapy, she developed similar symptoms. Repeat MRI showed progression of lesions. Further work-up including CSF Epstein-Barr virus PCR and SPECT Th 201 imaging was not conclusive for CNS lymphoma. The patient's clinical condition deteriorated and she died. We postulate that functional immunological dysfunction is a possible mechanism by which our patient developed TE despite demonstrating sustained immune response on ART.

Myocardial infarction with ST segment elevation (STE) on electrocardiography (ECG) is a common presentation in emergency rooms across the world. Myocardial injury and necrosis are infrequently the initial presentation in patients with thrombotic thrombocytopenic purpura (TTP). A 48-year-old woman presented with STE myocardial infarction from outside hospital for primary percutaneous coronary intervention. However, her clinical picture was not consistent. Rapid evaluation revealed symptoms associated with microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury with waxing and waning mental status. A diagnosis of TTP was made with low ADAMST-13 activity. Plasmapheresis was initiated along with intravenous steroid therapy. The patient had a full recovery and went home after full recovery of left ventricular ejection fraction and normal myocardial perfusion studies. Rapid evaluation is needed to identify infrequent causes of STE myocardial infarction. As swift protocols are activated in the emergency room and catheterization laboratories to ensure quality control, it is equally important to integrate all aspects of the patient's clinical and objective data to detect unusual disease entities.

No abstract

Patients presenting with acute heart failure (AHF) represent a heterogeneous population with respect to demographics, clinical profiles, and precipitating factors. Despite this, most clinical trials have treated the study population as a homogeneous group in an attempt to achieve adequate statistical power for endpoint analysis. This approach has proven to be of little value in the development of new agents for treatment of AHF. By contrast, the phase III clinical trial of relaxin focused on a subset of AHF patients who were normotensive or hypertensive and who had moderate renal impairment. The study patients, who were primarily from Eastern Europe, represented a population that would be expected to have less genetic variability than the study populations in larger multinational AHF trials. A focused study design targeting specific patient profiles should be considered for future clinical AHF trials that investigate new therapies or compare the effectiveness of existing therapies.

Background: Compared with medical therapy, percutaneous coronary intervention (PCI) does not reduce mortality or myocardial infarction in patients with stable angina. Therefore, PCI should be guided by refractory anginal symptoms and not just lesion characteristics. Hypothesis: We hypothesized that angiographic lesion characteristics and stress test results would have a greater role in the decision to proceed with PCI than would symptom severity. Methods: We performed a retrospective cohort study of patients undergoing elective cardiac catheterization and possible PCI at an academic medical center. Anginal symptoms, optimal medical therapy, antianginal therapy, stress test results, and angiographic lesions (including American College of Cardiology/American Heart Association [ACC/AHA] lesion type) were analyzed. Logistic regression was used to determine predictors of medical management among patients not referred for coronary artery bypass surgery. Results: Of the 207 patients with obstructive lesions amenable to PCI, 163 underwent PCI and 44 were referred to medical therapy. In the multivariable logistic model, the following variables were associated with medical management: advancing age (odds ratio [OR] There was no association with sex, race, symptoms, optimal medical therapy, maximal antianginal therapy, referral status, or type of interventional cardiologist (academic vs private practice). Conclusions: For patients undergoing cardiac catheterization for stable angina, the decision to proceed to PCI vs medical management appears to depend largely on patient and angiographic characteristics, but not on symptoms or ischemia. Distal and high-risk lesions (ACC/AHA type C) are more often referred for medical therapy.

Pulmonary artery catheters have been extensively used for hemodynamic assessment over the past several decades. We present a case that highlights the management of a known, but rare and catastrophic complication of pulmonary artery catheter based therapy. An elderly lady with acute decompensated heart failure, severe pulmonary hypertension, and atrial fibrillation on anticoagulation had a pulmonary artery catheter inserted for hemodynamic monitoring. Subsequently, the patient developed acute hemoptysis and damped pulmonary artery pressure waveforms during inflation of the catheter tip balloon. The possibility of pulmonary artery rupture was immediately recognized and confirmed with CT angiogram of the chest. Emergent interventional radiology guided coil embolization of pulmonary artery rupture and pseudoaneurysm was successful.

Advanced heart failure (HF) with persistent and progressive clinical decline despite maximal medical therapy portends a high mortality in the absence of advanced therapies, such as ventricular assist devices or heart transplantation. A subset of these advanced HF patients deteriorates into refractory cardiogenic shock, that is challenging to manage with vasoactive agents alone. Temporary mechanical circulatory support (MCS) device options have evolved over the years and provide a viable option to rescue and rest the myocardium of patients in cardiogenic shock. The goal of such therapy is to serve as bridge to recovery, or more often, a bridge to durable advanced therapies. For those patients with progressive advanced HF despite extensive medical therapy, durable MCS devices (ventricular assist devices) are available when heart transplantation is not feasible. In this article, we review currently available temporary and durable MCS devices, with a focus on their hemodynamic profiles, to inform optimal device selection for patients with advanced HF.