RESUMEN
Dystrophic cardiac calcification is often associated with conditions causing systemic inflammation and when present, is usually extensive, often encompassing multiple cardiac chambers and valves. We present an unusual case of dystrophic left atrial calcification in the setting of end stage renal disease on hemodialysis diagnosed by echocardiography and computed tomography. Significant calcium deposition is confined within the walls of the left atrium with no involvement of the mitral valve, and no hemodynamic effects.
RESUMEN
Thrombotic thrombocytopenia purpura (TTP) was first described in 1924 as a "pathologic alteration of the microvasculature, with detachment or swelling of the endothelium, amorphous material in the sub-endothelial space, and luminal platelet aggregation leading to compromise of the microcirculation". Ticlopidine induced TTP has been highly associated with autoimmune induced reduction in ADAMTS-13 activity. These findings, to a lesser extent, have also been found in clopidogrel induced TTP. We report a case of clopidogrel associated TTP in a patient that presented with acute stroke, renal failure, and non-ST elevation myocardial infarction.
RESUMEN
Ruptured sinus of Valsalva is very uncommon, and is < 1% of all congenital defects. The incidence ranges from 0.1%-3.5%. There is a male to female predominance of 4:1, with the highest incidence in the Asian population. Higher incidence is also seen in patients with Marfan's syndrome and Ehlers Danlos syndrome. There is a higher association of ruptured sinus of Valsalva with ventricular septal defect (VSD), aortic stenosis, and bicuspid valve defect. While most patients with VSD often have rupture of their right coronary sinus of Valsalva into the right ventricle due to poor structural integrity, we present a rare case of a patient with VSD who had rupture of his noncoronary sinus of Valsalva into the right atrium.
RESUMEN
Persistent left superior vena cava, usually an incidental finding, is the most common thoracic vein anatomical variation draining into the coronary sinus. Central venous catheter procedures may be complicated secondary to the presence of a persistent left superior vena cava, leading to life-threatening complications such as arrhythmias, cardiogenic shock, and cardiac arrest. We present a case of persistent superior vena cava diagnosed on transthoracic echocardiogram (TTE) in a patient with congestive heart failure. A dilated coronary sinus was identified on TTE, followed by injection of agitated saline into the left antecubital vein resulting in filling of the coronary sinus prior to the right atrium-an indication of persistent left superior vena-cava. This also was confirmed on cardiac computed tomography. Such a diagnosis is critical in patients who may undergo central venous catheter procedures such as our patient's potential requirement for an implantable cardiovertor defibrillator due to severe global left ventricular systolic dysfunction. The presence of a persistent left superior vena cava should always be suspected when the guidewire takes a left-sided downward course towards the right atrium at the level of the coronary sinus. Therefore, special attention should be paid to the imaging work-up prior to central venous catheter procedures.
RESUMEN
Pulsus alternans is characterized by regular rhythm with beat-to-beat alternation of systolic pressures. Left ventricular alternans is usually found in severe left ventricular dysfunction due to cardiomyopathy, coronary artery disease, systemic hypertension, and aortic stenosis. Right ventricular alternans is usually associated with left ventricular alternans, right ventricular dysfunction, pulmonary embolism, and pulmonary hypertension. Biventricular alternans is rare and associated with severe left ventricular dysfunction and left anterior descending coronary artery disease. The exact mechanism of pulsus alternans has not been clearly delineated, and it has been remained a subject of investigation and conjecture since the nineteenth century. Two fundamental mechanisms have been proposed to explain ventricular alteration. The first, based on the Frank-Starling mechanism, proposes beat-to-beat alteration in end-diastolic volume accounted for the alternating contractile force. The second proposed mechanism which explains the physiology of pulsus alternans involves the abnormal calcium handling by cardiac myocytes. To the best of our knowledge, biventricular alternans in pulmonary embolism has not been previously reported in the medical literature. We present and discuss the mechanisms of pulsus alternans and its clinical implications.