Patients with acute myocardial infarction may harbor multiple complex coronary plaques that are associated with adverse clinical outcomes. Plaque instability may be due to a widespread process throughout the coronary vessels, which may have implications for the management of acute ischemic heart disease.

In patients with right ventricular infarction, complete reperfusion of the right coronary artery by angioplasty results in the dramatic recovery of right ventricular performance and an excellent clinical outcome. In contrast, unsuccessful reperfusion is associated with impaired recovery of right ventricular function, persistent hemodynamic compromise, and a high mortality rate.

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Refractory no-reflow is associated with adverse outcomes in patients undergoing percutaneous coronary intervention. Charts were reviewed to identify 29 consecutive patients in whom intracoronary epinephrine was administered for refractory no-reflow. The effects of intracoronary epinephrine on coronary flow (TIMI grade), cardiac rhythm, and systolic blood pressure in the cardiac catheterization laboratory were assessed. Administration of intracoronary epinephrine (mean dose, 139 +/- 189 microg) resulted in significant improvement in coronary flow. After administration, TIMI 3 flow was established in 69% of patients. Overall, TIMI flow significantly increased (mean TIMI flow form 1.0 +/- 1.0 to 2.66 +/- 0.55; P = 0.0001). Intracoronary epinephrine resulted in significant but tolerable increase in heart rate (72 +/- 19 to 86 +/- 26 beats/min; P = 0.009), but no cases of acute dysrhythmia. These findings indicate that intracoronary epinephrine may exert salutary effects in patients suffering refractory no-reflow following elective or acute coronary interventions.

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Background-Although proximal right coronary artery (RCA) occlusion is the culprit commonly responsible for acute right ventricular (RV) infarction (RVI), the severity of RV dysfunction ranges broadly. This study was designed to delineate the patterns of coronary compromise that determine the magnitude of RV ischemic dysfunction. Methods and Results-In 125 patients with acute inferior myocardial infarction undergoing emergency angiography, the culprit infarct lesion was identified, RV branch flow assessed (TIMI flows and frame counts), and individual patient RV perfusion indices calculated by separately averaging the branch flows and frame counts, which were correlated with RV wall motion by ultrasound. RVI occurred in 53 (42%) patients, with the RCA as the culprit vessel and the lesion sufficiently proximal to compromise flow in at least one RV branch in all cases, thereby resulting in depressed RV perfusion (flow index, 0.7Ϯ0.2). In patients without RVI, the RCA was the culprit in 89%; the circumflex, in 11%. RCA culprits were proximal in 19% of such cases, with lack of RVI explained by preserved RV perfusion (flow index, 2.7Ϯ0.3; Pϭ0.001) attributable to at least 1 patent RV branch, spontaneous reperfusion, or prominent collaterals.Overall, there was a strong correlation between RV perfusion and wall motion (Spearman correlation coefficientϭ0.79). Conclusions-Proximal RCA occlusion compromising RV branch perfusion commonly results in RV ischemic dysfunction. In some cases with proximal RCA culprits, collaterals or spontaneous reperfusion preserve RV performance.

These data demonstrate that during right coronary artery occlusion and with reperfusion, bradycardia and hypotension develop more commonly in patients with proximal occlusions compared with those with distal occlusions. These findings suggest that reflexes arising from the ischemic right ventricle may play a role in bradyarrhythmias and hypotension.

The purpose of this study is to characterize the plaque morphology of severe stenoses in the superficial femoral artery (SFA) employing combined near-infrared spectroscopy and intravascular ultrasound (NIRS-IVUS). Atherosclerosis is the most common cause of symptomatic peripheral arterial disease. Plaque composition of SFA stenoses has been characterized as primarily fibrous or fibrocalcific by non-invasive and autopsy studies. NIRS has been validated to detect lipid-core plaque (LCP) in the coronary circulation. We imaged severe SFA stenoses with NIRS-IVUS prior to revascularization in 31 patients (46 stenoses) with Rutherford claudication ⩾ class 3. Angiographic parameters included lesion location and stenosis severity. IVUS parameters included plaque burden and presence of calcium. NIRS images were analyzed for LCP and maximum lipid-core burden index in a 4-mm length of artery (maxLCBI 4mm ). By angiography, 38 (82.6%) lesions were calcified and 9 (19.6%) were chronic total occlusions. Baseline stenosis severity and lesion length were 86.0 ± 11.0% and 36.5 ± 46.5 mm, respectively. NIRS-IVUS identified calcium in 45 (97.8%) lesions and LCP in 17 (37.0%) lesions. MaxLCBI 4mm was 433 ± 244. All lesions with LCP also contained calcium; there were no noncalcified lesions with LCP. In conclusion, this is the first study of combined NIRS-IVUS in patients with PAD. NIRS-IVUS demonstrates that nearly all patients with symptomatic severe SFA disease have fibrocalcific plaque, and one-third of such lesions contain LCP. These findings contrast with those in patients with acute coronary syndromes, and may have implications regarding the pathophysiology of atherosclerosis in different vascular beds.