Kenneth R. Bennett

Spontaneous migration of an inferior vena cava filter resulting in cardiac tamponade and percutaneous filter retrieval

Thromboembolic disease accounts for thousands of hospitalizations every year in the US. Its primary management consists of anticoagulation. However, in certain instances this may be contraindicated or not sufficient. Mechanic occlusion of the inferior vena cava (IVC) becomes then a viable alternative. In this case a 35‐year‐old man presented with a saddle pulmonary embolus but was unable to be anticoagulated due to intestinal bleed. A removable IVC filter was then placed. The filter spontaneously migrated into the right atrium causing severe tricuspid regurgitation, perforation of the atrial wall, and cardiac tamponade. The device was successfully retrieved percutaneously and the patient discharged from the hospital in stable condition. This case illustrates the potentially lethal complications associated with the use of IVC filters, as well as the possibility to percutaneously recover them from within the right atrium.

Adenosine infusion increases plasma levels of VEGF in humans.

BackgroundMany in vitro studies have shown that adenosine (Ado) can induce vascular endothelial growth factor (VEGF) mRNA and protein expression and stimulate endothelial proliferation. In the present study, we seek to determine whether Ado can increase circulating levels of VEGF protein in the intact human.MethodsFive outpatients 49.3 ± 6.7 years of age and weighing 88.2 ± 8.5 kg were selected. They were given a 6 min intravenous infusion of Ado (0.14 mg kg-1 min-1) in conjunction with sestamibi myocardial perfusion scans. Mean blood pressure (MBP, calculated from systolic and diastolic values) and heart rate (HR) were determined before Ado infusion and every 2 min for the next 10 min. Plasma VEGF concentrations (ELISA) were determined immediately before Ado infusion and 1 h, 2 h, and 8 h after the infusion.ResultsPlasma VEGF concentration averaged 20.3 ± 2.0 pg ml-1 prior to Ado infusion, and increased to 62.7 ± 18.1 pg ml-1 at 1 h post- infusion (p < 0.01). VEGF plasma concentration returned to basal levels 2 h after infusion (23.3 ± 3.4 pg ml-1). MBP averaged 116 ± 7 mmHg and heart rate averaged 70 ± 7 prior to Ado infusion. MBP decreased by a maximum of ~22% and HR increased by a maximum of ~17% during the infusion.ConclusionWe conclude from these preliminary findings that intravenous infusion of adenosine can increase plasma levels of VEGF in humans.

Correlation of myocardial 42 K uptake with coronary arteriography.

The myocardial uptake of potassium 42 was compared to the coronary arteriogram in 12 patients to evaluate the use of this method in detecting alterations in myocardial blood flow in patients with ischemic heart disease. Correlation was good in patients with occlusive lesions of the anterior descending artery; in patients with far-advanced coronary artery disease with extensive intercoronary collaterals; and in patients with akinetic or aneurysmal areas of the left ventricular free wall and apex.

Atraumatic Evaluation of Myocardial Revascularization Procedures with 43K1

Least-squares regression analysis was computerized to provide functional color images of myocardial perfusion patterns. In 8 of the 9 patients studied, changes in pattern indicated that the revascularization procedure speeded the appearance time and/or net rate of 43K uptake. The functional images correlated well with coronary arteriograms made before and after surgery. This noninvasive isotope technique may prove to be clinically useful in (a) evaluating coronary artery disease, (b) defining the remaining viable myocardium when an aneurysm is present, and (c) determining the effectiveness of the revascularization procedure.

Pulmonary arterial pressure method for estimating the ventricular stroke volume.

Surveillance of the pulmonary arterial (PA) and capillary wedge (PCW) pressures in coronary care units has been widely accepted as a safe and valuable procedure in the clinical management of acute myocardial infarction.1,2 The PA and PCW pressures provide a reasonable index of the left ventricular performance and serve as a useful guide in the therapeutic management of the patient. Work was undertaken for this report to determine if additional useful information could be derived from these measurements with a pulmonary arterial pressure method for estimating the right ventricular stroke volume.

Corrected transposition of the great arteries: A study of twelve cases

Abstract Twelve cases of corrected transposition of the great arteries are reviewed, and the clinical and laboratory features that can be helpful in making this diagnosis are discussed. Conduction disturbances, ventricular septal defects, pulmonary stenosis, patent ductus arteriosus and left atrioventricular valve regurgitation were the most commonly associated defects.

WITHDRAWN: Solve it Like Sherlock: Misplaced Electrodes

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Atypical Chest Pain—It's Time to Be Rid of It

u a c w t b m o F d b w i We have a problem that needs to be addressed. The empty phrase “atypical chest pain” has wormed its way into our lexicon, becoming so commonplace that someone unfamiliar with the subtleties of heart disorders might reasonably conclude that it’s a disease—complete with natural history, prognosis, and, heaven forbid, a treatment. The diagnosis of angina pectoris has always relied largely on the patient’s account, and traditional teaching holds that a physician should be able to make or exclude the diagnosis by the history alone. While this is often the case, there will always be those instances when the physician is hesitant to commit to a diagnosis. It is from such situations and our deep-seated desire to label the patient’s problem that we have the hedging terms “atypical angina,” “noncardiac chest pain,” and, sorry to say, “atypical chest pain.” Putting “atypical” aside, “chest pain” is vague enough— for without reference to cause, it leaves us in the dark, knowing only that it has something to do with the chest. Just mentioning that someone has chest pain immediately raises the specter of an ominous problem, namely coronary artery disease—even though we know that all chest discomforts aren’t cut from the same cloth, and many, if not most, have nothing to do with the heart. Unlike atypical chest pain, atypical angina (pectoris) and noncardiac chest pain really do mean something, with each conveying a sense of the physician’s thinking. Atypical angina implies that the complaint is actually angina pectoris, though not conforming in every way to the expected or classic description; noncardiac chest pain implies confidence that the problem doesn’t rest with the heart, whereas atypical chest pain says little more than there is something in or about the chest that bothers the patient, and to some extent concerns the physician, but which he or she is at a loss to explain or is unwilling to commit to a diagnosis— bluntly put, it can be caused by anything. Before coronary angiography, diagnosis of a patient’s chest complaint required little more than a physician’s opinion— there wasn’t much need for hedging. The diagnosis was what the doctor said it was, and who could say otherwise, because the means to confirm or refute the doctor’s opinion was limited to the electrocardiogram and perhaps some type of exercise test