p<0.005).And the decrease in tenting area with dobutamine had a good correlation with increase in Ssr in the inferior segment (r=0.62, p<0.01), but neither increase in Ssr in the anterior, anteroseptal, posteroseptal, posterior nor lateral segment.Furthermore, the decrease in MR volume fraction was correlated with increase in Ssr in the inferior segment (r=0.63, p<0.01). Conclusions:The results of this study suggest that inferior myocardial systolic function may affect the configuration of mitral apparatus and may be one of the determinants of functional MR severity.
In the acute coronary syndrome setting, the interaction between epicardial coronary artery stenosis and microcirculation subtended by the culprit vessel is poorly understood. The purpose of the present study was to assess the immediate impact of percutaneous coronary intervention (PCI) on microvascular resistance (MR) in patients with non-ST-elevation myocardial infarction (NSTEMI).Thirty-eight patients undergoing PCI for NSTEMI were recruited consecutively. Culprit lesions were stented over a Doppler and pressure-sensor-equipped guidewire. In the presence of epicardial stenosis, MR was calculated by taking collateral flow, as measured by the coronary wedge pressure, into consideration. After removal of epicardial stenosis, MR was calculated simply as distal coronary pressure divided by average peak velocity. When collateral flow was incorporated into the calculation, MR increased significantly from 1.70 ± 0.76 to 2.05 ± 0.72 (p=0.001) after PCI in the whole population. Periprocedural changes (Δ) in absolute values of MR and troponin T correlated significantly (r=0.629, p=0.0001). In patients who developed periprocedural myocardial infarction, MR increased significantly after PCI (1.48 ± 0.73 versus 2.28 ± 0.71, p<0.001). Nevertheless, removal of the epicardial lesion did not change MR in patients without periprocedural MI (1.91±0.73 versus 1.81±0.67, p=0.1).When collateral flow is accounted for, removal of epicardial stenosis increases MR in patients with NSTEMI undergoing PCI.
Aspirin resistance may increase the risk of major adverse cardiac events (MACE) more than threefold in patients with stable coronary artery disease (CAD). This study aimed to determine the prevalence of aspirin resistance in patients with stable CAD, the role of aspirin resistance on outcome in the follow-up, and the effect of clopidogrel therapy in MACE prevention in aspirin-resistant individuals. We detected the prevalence of aspirin resistance in 234 patients with stable CAD. Platelet function was determined by PFA-100 with collagen and/or epinephrine and collagen and/or ADP cartridges. The mean follow-up time was 20.6 +/- 6.9 months. The primary endpoints of the study were occurrence of myocardial infarction, unstable angina, stroke and cardiac death. Of patients, 22.2% (n = 52) were aspirin resistant by PFA-100. During follow-up, MACE occurred in eight patients (15.4%) with aspirin resistance and in 20 patients (11.0%) with aspirin-sensitive platelet aggregation (P = 0.269). MACE increased in aspirin-resistant patients after termination of clopidogrel therapy. Eleven patients experienced MACE after cessation of clopidogrel therapy (P < 0.001). The MACE risk in patients with stable CAD having detected aspirin resistance was similar compared with patients having aspirin-sensitive platelet aggregation by PFA-100. The MACE prevalence increased during follow-up, however, just after cessation of clopidogrel therapy.
Aspirin resistance could be defined as thrombotic and embolic cardiovascular events despite regular aspirin therapy. The study aimed to determine the profile and prevalence of aspirin resistance in coronary artery disease patients. We evaluated the prevalence of aspirin resistance in a cohort of 505 patients with the diagnosis of coronary artery disease taking 80–300 mg regular aspirin daily. Platelet functions were analyzed by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine cartridges and collagen and ADP cartridges. A closure time of 186 s or less with the collagen and epinephrine cartridge was defined as aspirin resistance. Of the patients, 118 (23.4%) were aspirin resistant by the PFA-100. Aspirin-resistant patients were more likely to be older than aspirin-sensitive patients (P = 0.024). No statistically significant differences between the aspirin-resistant and aspirin-sensitive individuals were present in gender, major risk factors of coronary artery disease, number and localization of involved coronary vessels, serum lipid levels, and blood counts. According to the high prevalence of coronary heart disease, many people are affected by aspirin resistance, which may play a role in adverse cardiovascular events. Monitoring of platelet function in patients with coronary heart disease may support the optimization of antiplatelet therapy with additional and/or alternative agents.
Essential thrombocythemia is a rare cause of ischemic cardiovascular events. A 23-year-old young man was admitted with chest pain to the coronary care unit. Electrocardiogram revealed acute anterior myocardial infarction (AMI). He had a platelet count 748,000/mm3 and detailed hematologic investigation led to the diagnosis of essential thrombocythemia. Coronary angiography revealed two vessel disease, with 95% stenosis in the middle of left anterior descending artery (LAD), thrombotic occlusion of distal LAD and recanalized thrombus in the right coronary artery (RCA). Apical akinesia and anterolateral hypokinesia was present by left ventriculography. In the same session, glycoprotein IIb/IIIa receptor antagonist drug (tirofiban) therapy was started and after 4 × 16 mm NIR primo stent was implanted in the middle of the LAD. With aspirin 300 mg/day and ticlopidine 500 mg/day therapy, platelet count was found to be around 530,000–550,000/mm3. Clinical follow-up of the patient showed no chest pain. Six months after angioplasty, stent in the LAD and distal of LAD was found to be open with control coronary angiography. Recanalized thrombus in RCA showed no difference. Medical follow up is decided. We decided to report this case since essential thrombocythemia is a rare disease that may result in serious life-threatening cardiovascular complication.