Arterial remodeling occurs in response to mechanical and neurohumoral stimuli. We hypothesized that veins, which are not exposed to higher pressures in hypertension, would demonstrate less active remodeling than arteries. We assessed remodeling with two standard measures of arterial remodeling: vessel morphometry and the expression/function of matrix metalloproteinases (MMPs). Thoracic aorta and vena cava from sham normotensive and DOCA-salt hypertensive rats (110 +/- 4 and 188 +/- 8 mmHg systolic blood pressure, respectively) were used. Wall thickness was increased in DOCA-salt vs. sham aorta (301 +/- 23 vs. 218 +/- 14 mum, P < 0.05), as was medial area, but neither measure was altered in the vena cava. The aorta and vena cava expressed the gelatinases MMP-2, MMP-9, transmembrane proteinase MT1-MMP, and tissue inhibitor of metalloproteinase-2 (TIMP-2). Immunohistochemically, MMP-2 localized to smooth muscle in the aorta and densely in endothelium/smooth muscle of the vena cava. Western and zymographic analyses verified that MMP-2 was active in all vessels and less active in the vena cava than aorta. In hypertension, MMP-2 expression and activity in the aorta were increased (59.1 +/- 3.7 and 74.5 +/- 6.1 units in sham and DOCA, respectively, P < 0.05); similar elevations were not observed in the vena cava. MMP-9 was weakly expressed in all vessels. MT1-MMP was expressed by the aorta and vena cava and elevated in the vena cava from DOCA-salt rats. TIMP-2 expression was significantly increased in the aorta of DOCA rats compared with sham but was barely detectable in the vena cava of sham or DOCA-salt hypertensive rats. These findings suggest that large veins may not undergo vascular remodeling in DOCA-salt hypertension.
Digoxin has been the cornerstone of the treatment of heart failure for more than 2 centuries. Now that newer therapies have been introduced that reduce the mortality rate in heart failure and recent trials have failed to prove the same for digoxin, its use has significantly decreased. But a careful review of the multiple pharmacologic actions of digoxin and closer analysis of the results of recent trials suggest that digoxin may in fact continue to be an effective treatment for heart failure.
Cholesterol crystal emboli triggered muscle inflammation and necrosis with an intact circulation. PET/CTA may help in the early detection of inflammation caused by CCs.
The prevalence of congenital coronary artery anomalies is approximately 1% in the general population. They are a common cause of sudden death in younger persons. The origination of the posterior descending artery (PDA) from left anterior descending (LAD) artery is an extremely rare anomaly. We present a case of a 54-year-old female who presented with diabetic ketoacidosis with co-existing non-ST elevation myocardial infarction, therefore, had an invasive angiogram that identified the anomalous origin of PDA from LAD. It is vital to define coronary anatomy as anomalies dictate which cardiac intervention should be attempted in cases of ischemia.
An atrial septal defect is the second most common congenital heart disease found in adults with a female to male ratio of 4 : 1. However, it is rare to have a complete absence of the interatrial septum (IAS) to be diagnosed in an elderly patient associated with other coexisting anomalies. We present a case of a 60-year-old female presenting with common atrium, coronary arteriovenous fistula, and coronary artery aneurysms. This case highlights rare adult congenital cardiac anomalies and the importance of thorough workup to evaluate for the intracardiac shunt in a patient who has right heart enlargement and development of pulmonary disease in adulthood without a significant history of chronic smoking. A 60-year-old female patient presented with substernal chest pain. The nuclear stress test showed no reversible ischemia; however, right ventricle (RV) dilation was present. The patient underwent further evaluation for RV dilation with a transthoracic echocardiogram that demonstrated a complete absence of IAS and was confirmed by a positive bubble study. The patient had an invasive angiography that showed severely elevated RV pressure. Oxygen saturation in the right atrium was higher than in the inferior vena cava. Hence, an intracardiac shunt with a 10% increase in oxygen saturation was identified. It also identified aneurysmal coronary arteries (measuring 0.8 to 1.0 cm). Cardiac computed tomography angiogram was performed that identified all coronary arteries to be ectatic/aneurysmal measuring up to 8-10 mm, an absence of IAS, and a possible fistula between the distal left anterior descending and a coronary vein. To our knowledge, this is the first-ever presentation of a complete congenital absence of IAS in a patient who has survived into adulthood with the development of severe pulmonary hypertension without Eisenmenger syndrome. It is unclear at this point if surgical treatment to correct the anatomical defect (which would be probably palliative) would be superior to conservative medical therapy. Besides, the presence of coronary arteriovenous fistula would make the decision-making process more complex regarding surgical versus conservative management.
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