Umamahesh C. Rangasetty

The cycloxygenase 2 (COX-2) story: it's time to explain, not inflame.

Despite initial promising reports that anti-inflammatory properties of cycloxygenase-2 (COX-2) inhibitors may confer anti-atherosclerosis effects and stabilize the atherosclerotic plaque, subsequent data from long-term clinical trials have shown that selective COX-2 inhibitors are associated with increased risk of cardiovascular events. The commonly cited explanation is that selective inhibition of COX-2 leads to depletion of prostacyclin, whereas the production of pro-thrombotic thromboxane by means of cycloxygenase-1 (COX-1) is unopposed. This hypothesis seems unlikely as the overall explanation, because low-dose aspirin does not decrease the increased risk associated with COX-2 inhibitors. Moreover, the risk associated with nonselective COX inhibitors may be similar to selective COX-2 inhibitors. Alternative hypotheses include (1) elevated blood pressure, (2) abnormal vascular remodeling, (3) inhibition of protective mechanisms against ischemia—reperfusion injury, and (4) inhibition of 15-epi-lipoxin production. Varying results in different experimental models may be related to the fact that COX-2 is involved in numerous cellular functions. Inhibiting COX-2 in inflammatory cells may have favorable effects, whereas in organs such as the heart and brain and/or blood vessels may have deleterious effects. Currently, the “selective COX-2 inhibitors” are not selective in the sense that they inhibit COX-2 in all tissues without predilection to inflammatory cells and, as a result, may summate to increase the risk of cardiovascular events.

Cardiac allograft vasculopathy: advances in diagnosis.

Cardiac allograft vasculopathy (CAV), characterized by diffuse intimal thickening and luminal narrowing in the arteries of the allograft, is the leading cause of morbidity and mortality in cardiac transplant recipients. Many transplant centers perform routine annual surveillance coronary angiography. However, angiography can underdiagnose or miss CAV due to its diffuse nature. Intravascular ultrasound (IVUS) is more sensitive than angiography. IVUS provides not only accurate information on lumen size, but also quantification of intimal thickening, vessel wall morphology, and composition. IVUS has evolved as a valuable adjunct to angiography and the optimal diagnostic tool for early detection. Noninvasive testing such as dobutamine stress echocardiography and nuclear stress test have shown considerable accuracy in diagnosing significant CAV. Computed tomographic imaging and cardiac magnetic resonance imaging are promising new modalities but require further study. This article reviews the diagnostic methods that are currently available.

Tolvaptan: a selective vasopressin type 2 receptor antagonist in congestive heart failure

The neurohormone arginine vasopressin plays a significant role in the regulation of volume homeostasis, which is mediated via vasopressin type 2 (V2) receptors in the collecting tubules of the kidney. Diseases that are accompanied by abnormal volume homeostasis, including congestive heart failure and cirrhosis, are a frequent cause of hospital admissions and increasing healthcare costs. Recently, several nonpeptide V2 receptor antagonists have emerged as promising agents in the management of these conditions with the advantage of having no electrolyte abnormalities, neurohormonal activation or worsening renal insufficiency. Tolvaptan, a highly selective nonpeptide V2 receptor antagonist, has demonstrated an improvement in the volume status, osmotic balance and haemodynamic profile in preclinical and Phase II trials in patients with congestive heart failure and is currently undergoing testing in Phase III trials. This review discusses the evidence for the potential uses of tolvaptan, and its pharmacology and pharmacokinetics, particularly in congestive heart failure.

Reversible right ventricular dysfunction in patients with HIV infection.

Human immunodeficiency virus-related cardiomyopathy is characterized by global left ventricular (LV) dysfunction commonly associated with biventricular dilation. Human immunodeficiency virus (HIV) cardiomyopathy carries a poor prognosis, and the role of antiretroviral therapy in the reversal of heart failure is not very clear. We report two patients with HIV infection who presented with severe right ventricular (RV) dysfunction in the absence of pulmonary parenchymal, pulmonary arterial and left ventricular myocardial involvement. During the period of intensive antiretroviral therapy, the symptoms of right heart failure progressively and remarkably improved. This was accompanied by normalization of right ventricular size and RV function documented by repeat echocardiograms. Given that the serologic tests for opportunistic infections were negative, and the RV function improvement correlated with a decrement in the viral load, it is likely that the cardiomyopathy was due to direct infection by HIV. These cases illustrate that there can be isolated involvement of the right heart in the absence of lung, significant pulmonary vascular and left ventricular disease, and also that the antiretroviral therapy might reverse the cardiomyopathy.

Transcatheter Closure of Coronary-to-Pulmonary Fistula by Nonconventional Coils in a Patient with Tetralogy of Fallot

We report a case in which a coronary-to-pulmonary fistula was successfully occluded in a patient with tetralogy of Fallot by employing the cut floppy tips of coronary angioplasty guidewires using a new technique.

Imaging in heart failure: role of preoperative imaging and intraoperative transesophageal echocardiography for heart failure surgery.

The prevalence of chronic heart failure continues to increase with over 500,000 new cases diagnosed each year. This is largely due to improved survival and an aging population. Recent advances in imaging techniques have improved the diagnostic accuracy and resulted in earlier diagnoses of heart failure. These imaging techniques include echocardiography, nuclear cardiac imaging, computerized tomographic angiography and cardiac magnetic resonance imaging. Anesthesiologists involved in the care of heart failure patients should have adequate knowledge to review and understand the results of all preoperative cardiac investigations. At the time of presentation, they may find that patients with a history of heart failure have undergone several noninvasive imaging techniques to quantify coronary stenosis, measure ventricular function, diagnose valvular pathology and evaluate the viability of myocardium. This information is important when making decisions related to perioperative hemodynamic management and surgical planning. Echocardiography is unique in its usefulness for both

Contrast-Enhanced Echocardiography in Spindle Cell Sarcoma of the Pericardium

A 37-year-old male was admitted from the emergency department for evaluation of symptoms of congestive heart failure. He presented having experienced atypical chest pain, progressive dyspnea, and swelling of the legs for 2 weeks. Physical examination was notable for tachycardia, elevated jugular venous pressure, muffled heart sounds, and bilateral pitting pedal edema. An ECG showed sinus tachycardia and low-voltage complexes, and chest x-ray revealed cardiomegaly. A 2-dimensional echocardiogram was done to evaluate cardiac chambers and left ventricular function. Surprisingly, it showed compression of the right atrium and right ventricle by a large mass possibly originating from the pericardium, dilated inferior vena cava, no significant respiratory variation in transmitral and tricuspid Doppler velocities, and expiratory reversal of flow in the hepatic veins. A contrast echocardiogram was performed to further assess the cardiac chambers …

Percutaneous closure of coronary pulmonary arterial fistula using catheterization laboratory trash

We report a case of coronary pulmonary arterial fistula that was successfully occluded by packing the fistula with thrombogenic floppy tips of used percutaneous transluminal coronary angioplasty guidewires instead of conventional steel coils. Cathet Cardiovasc Intervent 2003;59:49–51.

Late diagnosis of Wellens syndrome in a patient presenting with an atypical acute coronary syndrome

Atypical myocardial infarctions (MI) are one of the more feared diagnoses among cardiologists, emergency department physicians, and internists for patients presenting with presumed non-cardiac chest pain. Delays in care for patients presenting with atypical MIs can lead to increases in morbidity and mortality. This is also true in the case of Wellens’ syndrome where delays in coronary revascularization can also lead to left ventricular dysfunction and death. Here, we report the case of a 48 year old man with no known risk factors for coronary disease who presents with atypical symptoms, a very late rise in serum troponin, and ECG changes consistent with Wellens’ syndrome as part of an acute nonST elevation myocardial infarction (NSTEMI).

A perfect host.

A 42-year-old prison inmate with a history of acquired immune deficiency syndrome (AIDS) was admitted with abdominal pain and haematemesis. Laboratory examination showed a white cell count of 13.7 10/L, with 40% eosinophils and a CD4 count of 11 10/L. Stool studies showed hookworm ova and Strongyloides stercoralis larvae. Gastroduodenoscopy showed gastritis, severe nodular duodenitis (Fig. 1) and a worm-like structure measuring 10 cm in length in the duodenum (Fig. 2). Gastric and duodenal biopsies were positive for Strongyloides (Fig. 3). He was treated with albendazole and ivermectin before discharge. One month later, he presented with recurrent haematemesis and pneumonia requiring mechanical ventilation. Stool studies and gastric–duodenal biopsies again showed Strongyloides. Expectorated sputum was also positive for Strongyloides. Ivermectin was given for 2 weeks with complete resolution of symptoms. Stool studies at 1 month follow up were negative. S. stercoralis is an intestinal nematode that inhabits the human small intestine. S. stercoralis is unique among intestinal nematodes in its ability to complete its life cycle within the host through an asexual autoinfective cycle, allowing the infection to persist in the host indefinitely. Under some conditions associated with immunocompromise, whether iatrogenic (corticosteroids, chemotherapeutic agents) or disease related, this autoinfective cycle can become amplified into a potentially fatal hyperinfection syndrome. The clinical findings in the hyperinfection syndrome may be attributable to the direct consequences of organ invasion by the filariform larvae