Abhiram Prasad

Smoking Is Associated With Epicardial Coronary Endothelial Dysfunction and Elevated White Blood Cell Count in Patients With Chest Pain and Early Coronary Artery Disease

Background— Smoking is a major risk factor for cardiovascular events. One of the potential mechanisms may be related to both coronary endothelial dysfunction and increased inflammatory response. The present study was designed to test the hypothesis that smoking is associated with epicardial coronary endothelial dysfunction and inflammation. Methods and Results— Coronary endothelial function in response to acetylcholine was assessed in 881 patients (115 current smokers and 766 nonsmokers, including 314 previous smokers). Smokers were significantly younger than nonsmokers (43±1 versus 51±1 years, P<0.0001), had more epicardial vasoconstriction in response to intracoronary acetylcholine (−19±2% versus −14±1% change in coronary artery diameter, P=0.03), and were more likely than nonsmokers to have epicardial endothelial dysfunction (46% versus 35%, P=0.005), but their microvascular endothelial function was intact. Smokers had higher white blood cell counts than nonsmokers (7.7±0.2 versus 6.6±0.1×109/L, P<0.0001), higher myeloperoxidase (156±19 versus 89±8 ng/mL), higher lipoprotein-associated phospholipase A2 (242±12 versus 215±5 ng/mL), and higher levels of intracellular adhesion molecule (283±14 versus 252±5 ng/mL). There were no differences in the levels of C-reactive protein, fibrinogen, or vascular cell adhesion molecule between the groups. Conclusion— Young smokers are characterized by epicardial coronary endothelial dysfunction, preserved microvascular endothelial function, and increased levels of inflammatory biomarkers and oxidative stress. The present study provides further information regarding the potential mechanisms by which smoking contributes to cardiovascular events.

“Familial” apical ballooning syndrome (Takotsubo cardiomyopathy)

We present a case of a 44 year-old woman who was diagnosed with apical ballooning syndrome (ABS). She reported that her family history consisted of her mother suffering a myocardial infarction at the age of 49 years. The mother had been told that she had normal coronary arteries and was treated for coronary artery spasm. We reviewed the medical records, coronary angiogram and left ventriculogram of the mother, and concluded that she too had suffered an episode of ABS which had been diagnosed as a myocardial infarction. Our observation of a familial clustering of ABS has two important implications. First, it suggests that there may be a genetic predisposition for the cardiomyopathy which may explain why only a minority of postmenopausal women appear to be susceptible. Second, it illustrates that despite the apparent recent emergence of the syndrome, it did occur in the past.

Lack of Correlation Between Noninvasive Stress Tests and Invasive Coronary Vasomotor Dysfunction in Patients With Nonobstructive Coronary Artery Disease

Background—Despite a nonobstructive coronary angiogram, many patients may still have an abnormal coronary vasomotor response to provocation and to myocardial demand during stress. The ability of noninvasive stress tests to predict coronary vasomotor dysfunction in patients with nonobstructive coronary artery disease is unknown. Methods and Results—All patients with nonobstructive coronary artery disease who had invasive coronary vasomotor assessment and a noninvasive stress test (exercise ECG, stress echocardiography, or stress nuclear imaging) within 6 months of the cardiac catheterization with provocation at our institution were identified (n=376). Coronary vasomotor dysfunction was defined as a percentage increase in coronary blood flow of ≤50% to intracoronary acetylcholine (endothelium-dependent dysfunction) and/or a coronary flow reserve ratio of ≤2.5 to intracoronary adenosine (endothelium-independent dysfunction). We determined the sensitivity and specificity of various noninvasive stress tests to predict coronary vasomotor dysfunction in these patients. On invasive testing, 233 patients (63%) had coronary vasomotor dysfunction, of which 187 patients (51%) had endothelium-dependent dysfunction, 109 patients (29%) had endothelium-independent dysfunction, and 63 patients (17%) had both. On noninvasive stress testing, 157 (42%) had a positive imaging study and 56 (15%) a positive ECG stress test. The noninvasive stress tests had limited diagnostic accuracy for predicting coronary vasomotor dysfunction (41% sensitivity [95% CI, 34 to 47] and 57% specificity [95% CI, 49 to 66]), endothelium-dependent dysfunction (41% sensitivity [95% CI, 34 to 49] and 58% specificity [95% CI, 50 to 65]), or endothelium-independent dysfunction (46% sensitivity [95% CI, 37 to 56] and 61% specificity [95% CI, 54 to 67]). The exercise ECG test was more specific but less sensitive than the imaging tests. Conclusion—This study suggests that a negative noninvasive stress test does not rule out coronary vasomotor dysfunction in symptomatic patients with nonobstructive coronary artery disease. This underscores the need for invasive assessment or novel more sensitive noninvasive imaging for these patients.

Acute myocardial infarction due to left circumflex artery occlusion and significance of ST-segment elevation.

Acute occlusion of the left circumflex (LC) artery can be difficult to diagnose. The aim of the present study was to assess the incidence of LC occlusion in patients with acute myocardial infarction (AMI) requiring percutaneous coronary intervention (PCI), the frequency of ST-segment versus non-ST-segment elevation presentation among them, and to correlate the electrocardiographic findings with the outcomes. The clinical characteristics and outcomes of consecutive patients from November 2001 through December 2007 with AMI within 7 days before PCI of a single acutely occluded culprit vessel were included in the present analysis. Of the 1,500 patients, the culprit lesion was located in the right coronary artery, left anterior descending artery, or LC artery in 44.7%, 35.8%, and 19.5% of patients, respectively. Of the 1,500 patients, 72% presented with ST-segment elevation AMI, but only 43% were patients with a LC lesion (n = 127). PCI was significantly less likely (80%, 83%, and 70% for right coronary, left anterior descending, and LC artery, respectively; p < 0.001) to be performed within 24 hours for LC occlusions than for occlusions in the other territories. Among those with a non-ST-segment elevation AMI, the highest post-PCI troponin levels were in patients with a LC artery occlusion (median 1.4, 1.3, and 2.5 ng/ml; p < 0.001). No significant difference was found in the in-hospital mortality (4.4%, 7.4%, and 6.5%; p = 0.66) or major adverse cardiovascular event (9.2%, 13.9%, and 11.6%; p = 0.53) rates for right, left anterior descending, and LC occlusions, respectively. In conclusion, our results have demonstrated that in clinical practice, the LC artery is the least frequent culprit vessel among patients treated invasively for AMI. Patients with LC occlusion are less likely to present with ST-segment elevation AMI and have emergency PCI. The study results suggest that detection of these patients has been suboptimal, highlighting the need to improve the diagnostic approach toward the detection of an acutely occluded LC artery.