Jason N. Salamon

Patent foramen ovale: Unanswered questions.

The foramen ovale is a remnant of the fetal circulation that remains patent in 20-25% of the adult population. Although long overlooked as a potential pathway that could produce pathologic conditions, the presence of a patent foramen ovale (PFO) has been associated with a higher than expected frequency in a variety of clinical syndromes including cryptogenic stroke, migraines, sleep apnea, platypnea-orthodeoxia, deep sea diving associated decompression illness, and high altitude pulmonary edema. A unifying hypothesis is that a chemical or particulate matter from the venous circulation crosses the PFO conduit between the right and left atria to produce a variety of clinical syndromes. Although observational studies suggest a therapeutic benefit of PFO closure compared to medical therapy alone in patients with cryptogenic stroke, 3 randomized controlled trials (RCTs) did not confirm the superiority of PFO closure for the secondary prevention of stroke. However, meta-analyses of these RCTs demonstrate a significant benefit of PFO closure over medical therapy alone. Similarly, observational studies provide support for PFO closure for symptomatic relief of migraines. But one controversial randomized study failed to replicate the results of the observational studies while another two demonstrated a partial benefit. The goal of this review is to discuss the clinical conditions associated with PFO and provide internists and primary care physicians with current data on PFO trials, and clinical insight to help guide their patients who are found to have a PFO on echocardiographic testing.

Relaxin levels in pulmonary hypertension: a comparison between pulmonary arterial hypertension and diastolic heart failure-induced pulmonary hypertension.

Jeremy A. Mazurek, MD, Benjamin D. Horne, PhD, MPH, Iosif Kelesidis, MD, Jason N. Salamon, MD, and Ronald Zolty, MD, PhD From the Department of Medicine, Cardiovascular Division, Hospital of the University of Pennsylvania, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania; Intermountain Heart Institute, Intermountain Medical Center, Salt Lake City, Utah; Department of Medicine, Division of Cardiology, Montefiore Medical Center; and the Department of Medicine, Jacobi Medical Center, Albert Einstein College of Medicine, Bronx, New York

THE RED CELL DISTRIBUTION WIDTH AND THE CBC RISK SCORE MEASURED PRIOR TO LEFT VENTRICULAR ASSIST DEVICE IMPLANTATION PREDICT POST-IMPLANT SURVIVAL

The red cell distribution width (RDW) predicts mortality in many cardiovascular (CV) diseases. The sex-specific complete blood count (CBC) risk score uses the RDW and other CBC components to predict mortality. Very few risk models are known for predicting survival in patients undergoing left

Systemic mastocytosis presenting as cardiac tamponade with CD25+ pericardial mast cells

In this first‐in‐literature case, we describe a patient with Systemic mastocytosis presenting with life‐threatening cardiac tamponade associated with the presence of aberrant mast cells in the pericardium. Procedures involving surgical incisions through the pericardium in such cases can lead to uncontrolled mast cell degranulation leading to circulatory collapse.

ENDOTHELIN-1 LEVELS IN PULMONARY HYPERTENSION: A COMPARISON BETWEEN PULMONARY ARTERIAL HYPERTENSION AND DIASTOLIC HEART FAILURE-INDUCED PULMONARY HYPERTENSION

Endothelin-1 (ET-1), a potent vasoconstrictor, is elevated in heart failure states as well as in pulmonary arterial hypertension (PAH). Additionally, ET-1 receptor blockade is a mainstay of PAH treatment. Diastolic heart failure (DHF) is a common cause of secondary pulmonary hypertension (D-PH), and

CLINICAL IMPROVEMENT IN PATIENTS WITH EXERCISE INDUCED PULMONARY ARTERY HYPERTENSION AFTER 6 MONTHS OF PHOSPHODIESTERASE-5 INHIBITORS OR ENDOTHELIAL RECEPTOR ANTAGONISTS OR BOTH

Pulmonary arterial hypertension (PAH) is a rapidly progressive disorder with high mortality rates despite traditional medical treatment. With the availability of PA targeted therapy, early PAH detection improves treatment outcomes. Exercise- induced Pulmonary Artery Hypertension (EiPAH) represents

CLINICAL IMPROVEMENT IN PATIENTS WITH EXERCISE INDUCED PULMONARY ARTERY HYPERTENSION IS SIMILAR TO PULMONARY ARTERIAL HYPERTENSION

Exercise-induced Pulmonary Artery Hypertension (EiPAH) represents an early phase of Pulmonary Arterial Hypertension (PAH) in which screening and early detection might facilitate treatment aimed at preventing progression of EiPAH to resting PAH. In this study we sought to compare change in 6MWD after

Quite a backup: pericardial varices in a patient with hereditary antithrombin deficiency.

A 39 year-old female with known hypertension, gastro-esophageal reflux disease, and hereditary anti-thrombin deficiency (hATD) on life-long anti-coagulation presented to our emergency room with acute atypical chest and epigastric pain. Her hATD was diagnosed five years prior when repeated deep vein thromboses were discovered. At that time, the patient was started on life-long anticoagulation with warfarin and was able to consistently achieve therapeutic levels.

STIMULATION OF PULMONARY ARTERIAL ENDOTHELIUM IN DIASTOLIC HEART FAILURE INDUCED PULMONARY HYPERTENSION SIMILAR TO PULMONARY ARTERIAL HYPERTENSION

Background: Von Willebrand Factor (vWF) is secreted by the endothelium at elevated levels with endothelial dysfunction. Diastolic heart failure is the most common cause of secondary pulmonary hypertension (DHF-PH). In vitro, similar to PAH, DHF-PH has additional pre-capillary active pro-inflammatory changes. However, there is no evidence of in-vivo localized endothelial dysfunction in DHF-PH. We compared levels of pulmonary arterial (PA) vWF Ag and factor VIII (F8) in patients with both PAH and DHF-PH.

Postmenopausal Women with Constipation and Cardiovascular Disease

The secondary analysis of the Women’s Health Initiative’s observational arm by Salmoirago-Blotcher et al offers a novel approach to the risk factors associated with this disease. This study clearly documents the distribution of the many cardiovascular risk factors, such as smoking and diabetes. Although the study does document the use of symptomatic medications such as diuretics and calcium channel blockers, it would be helpful to know the distribution of mortality-reducing medications in post-cardiovascular injury, such as angiotensin-converting enzyme inhibitors, beta-blockers, and aspirin. Furthermore, compared with other lipid-lowering agents, statins have been shown to decrease mortality in cardiovascular disease via their direct low-density lipoprotein-reducing and pleiotropic anti-inflammatory effects. It would be informative to know how many of the study patients are specifically taking statins. Including these medications in the study’s statistical analyses will increase the power and clinical application of the authors’ conclusion. An additional connection that may support their findings is the altered neurohormonal milieu that has been found in both irritable bowel syndrome and heart disease. Specifically, serotonin levels have been found to be elevated in both irritable bowl syndrome and cardiovascular disease. In cardiovascular disease, the release f serotonin by activated platelets leads to vasoconstriction and ncreased smooth muscle cell aggregation, while in irritable owel syndrome, enterochromaffin cells produce and secrete seotonin, stimulating both local and central pathways. In both diseases, targeting serotonin, either directly or indirectly, has shown evidence of altering serotonin levels and possibly the course of disease. Further research linking the pathophysilogy of these 2 diseases may offer novel understandings and herapeutic interventions.