The role of angiographic follow-up after percutaneous coronary intervention.

In the early days of coronary angioplasty, follow-up coronary angiography was often performed to assess restenosis. Angiographic restenosis has been shown to be associated with worse clinical outcomes, though the exact causality has yet to be determined. Numerous studies have repeatedly demonstrated that routine follow-up coronary angiography increases the incidence of target lesion revascularization without a clear reduction in mortality or myocardial infarction. Despite the lack of proven benefit of angiographic follow-up, routine follow-up coronary angiography is still being performed in certain countries and facilities. There are several factors that might explain the lack of benefit of angiographic follow-up: 1) lower incidence of stent failure in the current drug-eluting stent era has attenuated the net clinical benefit of follow-up angiography. 2) Angiographic restenosis might not lead to myocardial ischemia. 3) Patients that do have functionally significant restenosis are often referred for coronary angiography due to clinical indications such as intractable angina. 4) Absence of restenosis at the time of follow-up angiography does not exclude future restenosis. The absence of proven benefit in unselected populations does not necessarily preclude the presence of benefit in selected population, and there may be a subgroup of patients who can benefit from angiographic follow-up such as those with a large myocardial ischemic territory or those at very high risk of restenosis. Until there is more clinical evidence with respect to follow-up angiography, the decision of whether or not to perform it routinely in selected high-risk population should entail an in-depth discussion with the patient.

Electrocardiographic Left Ventricular Hypertrophy as a Predictor for Nonsignificant Coronary Artery Disease in Patients With Non-ST-Segment Elevation Myocardial Infarction.

Left ventricular hypertrophy (LVH) can lead to subendocardial ischemia by altering the coronary blood flow and its transmural myocardial distribution in the setting of increased oxygen demand. We hypothesized that electrocardiographic LVH predicts nonsignificant coronary artery disease (CAD) in patients with non-ST-segment elevation myocardial infarction (NSTEMI). We performed a retrospective analysis of 406 consecutive patients with NSTEMI who underwent coronary angiography. The LVH was diagnosed using Sokolow-Lyon and Cornell voltage criteria. Nonsignificant CAD was defined as stenosis less than 50% in the left main and 70% in any other coronary arteries. Of the 406 patients, 100 (25%) patients had electrocardiographic LVH and 99 (24%) patients had nonsignificant CAD. Patients with electrocardiographic LVH had a higher prevalence of nonsignificant CAD (32% vs 22%, P = .04) and a lower rate of in-hospital revascularization (45% vs 69%, P < .001) than those without LVH. On multivariate analysis, electrocardiographic LVH was an independent predictor of nonsignificant CAD (odds ratio 1.94; 95% confidence interval 1.12-3.35; P = .02). In conclusion, electrocardiographic LVH is an independent predictor of nonsignificant CAD and associated with a lower rate of in-hospital revascularization in patients with NSTEMI.

Association Between Preinfarction Angina and Angiographic Findings in Non-ST-Segment Elevation Myocardial Infarction.

BACKGROUND: The association between preinfarction angina and angiographic findings has not been elucidated in patients with non-ST-segment elevation myocardial infarction (NSTEMI). HYPOTHESIS: Patients with preinfarction angina have favorable angiographic findings. METHODS: This retrospective study analyzed 481 patients who underwent coronary angiography within 5 days of presenting NSTEMI. Preinfarction angina was defined as experiencing ≥1 chest-pain episode within 7 days prior to admission. Infarct size was measured as the peak cardiac troponin I (cTnI) level, and large myocardial infarction (MI) was defined as a peak cTnI level >85th percentile value in the study population. Infarct-related artery (IRA) patency was defined as Thrombolysis In Myocardial Infarction grade 2 or 3 flow. Clinical and angiographic characteristics and in-hospital mortality were compared between patients with and without preinfarction angina. RESULTS: Among 481 patients, 200 (42%) had preinfarction angina. Preinfarction angina was associated with smaller infarct size, indicated by lower peak cTnI levels (P = 0.006) and lower incidence of large MI (P = 0.02), and IRA patency (P = 0.03). There was no significant difference in in-hospital mortality. On multivariate analysis, both preinfarction angina (odds ratio: 0.53, 95% confidence interval: 0.29-0.94, P = 0.03) and IRA patency (odds ratio: 0.30, 95% confidence interval: 0.17-0.52, P < 0.001) were independent negative predictors of large MI. CONCLUSION: Our study demonstrates that preinfarction angina is a predictor of smaller infarct size and infarct-related artery patency in NSTEMI patients, suggesting that NSTEMI patients presenting without preinfarction angina are at increased risk of developing a large MI.

Neutrophil-to-lymphocyte ratio as an independent predictor of left main and/or three-vessel disease in patients with non-ST-segment elevation myocardial infarction.

BACKGROUND/PURPOSE: Patients with acute coronary syndrome due to left main and/or three-vessel disease (LM/3VD) are at the highest risk of short- and long-term adverse cardiovascular events. Neutrophil-to-lymphocyte ratio (NLR) has been shown to predict the severity of coronary artery disease in various clinical settings, but its independent predictive value for LM/3VD has not been investigated in patients with non-ST-segment elevation myocardial infarction (NSTEMI). We aimed to evaluate the independent predictive value of NLR for LM/3VD in NSTEMI patients. METHODS/MATERIALS: We performed a retrospective analysis of consecutive NSTEMI patients who underwent coronary angiography. NLR was calculated as the ratio of neutrophil to lymphocyte based on the laboratory data on admission. The primary outcome was the presence of LM/3VD. RESULTS: In all, 396 patients were included in the final analysis. Median NLR in the entire study population was 3.43 (interquartile range, 2.12-5.51). By receiver operating characteristics curve analysis, the optimal cutoff value of NLR in predicting LM/3VD was 2.80 (area under the curve 0.60, sensitivity 73%, specificity 43%). Of the 396 patients, 244 patients (62%) had NLR ≥2.8. Patients with NLR ≥2.8 were older and had a higher prevalence of LM/3VD (30 % vs. 18%, p=0.005). According to multivariate logistic regression analysis, NLR ≥2.8 was an independent predictor of LM/3VD after adjusting for other clinical variables including ST depression and ST elevation in lead aVR (odds ratio 1.83, 95% confidence interval 1.07-3.21, p=0.03). CONCLUSION: Our study demonstrates that NLR ≥2.8 is an independent predictor of LM/3VD in patients with NSTEMI.

Prevalence and outcomes of non-ST-segment elevation myocardial infarction resulting from stent thrombosis.

BACKGROUND/PURPOSE: Stent thrombosis is an infrequent yet one of the most feared complications after stent implantation. Stent thrombosis most commonly manifests as ST-segment elevation myocardial infarction, thus the data regarding non-ST-segment elevation myocardial infarction (NSTEMI) resulting from stent thrombosis are still sparse. The aim of the study is to evaluate the prevalence and outcomes of NSTEMI resulting from stent thrombosis. METHODS/MATERIALS: We performed a retrospective analysis of 378 consecutive NSTEMI patients who underwent coronary angiography. Patients were divided into those with and without stent thrombosis. The primary outcome was in-hospital mortality. Secondary outcome was the incidence of large myocardial infarction defined as a peak troponin I value greater than 90th percentile of the entire study population (26.5 µg/L). RESULTS: Among 378 patients with NSTEMI, 12 (3.2%) patients had angiographically confirmed definite stent thrombosis. With respect to the timing of stent thrombosis, 2 patients had early, 3 had late and 7 had very-late stent thrombosis. Patients with stent thrombosis had a higher incidence of large myocardial infarction (33% vs. 9%, p = 0.02) and a higher albeit statistically insignificant peak troponin value (interquartile, 4.62 [0.19-64.0] µg/L vs. 1.21 [0.14-7.12] µg/L, p = 0.25) compared to those without stent thrombosis. There was no significant difference in in-hospital mortality between the two groups (8% vs. 2%, p = 0.2). CONCLUSIONS: Stent thrombosis accounted for 3.2% cases of NSTEMI in our cohort of patients and patients with NSTEMI resulting from stent thrombosis had a higher incidence of large myocardial infarction.