No abstract

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 (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.

Coronary microvascular disease or dysfunction (CMVD) has been associated with adverse cardiovascular outcomes. Despite a growing prevalence, guidelines on definitive treatment are lacking. Proposed mechanisms of endothelial dysfunction and resultant inflammation have been demonstrated as the underlying cause. Imaging modalities such as echocardiography, cardiac MRI, PET, and in some instances CT, have been shown to be useful in diagnosing CMVD mainly through assessment of coronary blood flow. Invasive measurements through thermodilution and pressure sensor-guided Doppler microcatheters have also been utilized. Treatment options are directed at targeting inflammatory pathways and angina. In our review, we highlight the current literature on the background of CMVD, diagnostic modalities, and management of this disease.

Figure 1. Echocardiogram in parasternal short-axis view showing (arrow) dilated origin of left main coronary artery. AO = aorta; LA = left atrium. 213 × 254 mm (96 × 96 DPI).murmur in the left parasternal area. Patient's electrocardiogram was normal and chest x-ray showed cardiomegaly. Two-dimensional echocardiography in the short axis revealed a dilated left main coronary artery ( Fig. 1). Color Doppler showed a turbulent jet originating from the left main coronary artery and draining into the right atrium (Fig. 2). A tortuous fistulous tract was seen coursing posterior and draining into the right atrium by two separate openings one below the other (Fig. 3). Just before the communication the fistula was aneurysmal (Fig. 3). Selective left coronary artery injection showed a large fistula originating from the dilated left main coronary artery and was draining into the right atrium (Fig. 4). Anatomy of the fistula was similar to the one demonstrated by the Figure 2. Color Doppler imaging in apical five chamber view showing turbulent color flow originating from the left main coronary artery, coursing behind the left atrium before draining into the right atrium. AO = aorta; LA = left atrium; and RA = right atrium. 168 × 129 mm (96 × 96 DPI).