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Introduction: Insufficient inhibition of platelets in patients with atherosclerosis despite antiplatelet therapy leads to important clinical consequences. The present study evaluated the role of vitamin D (VD) deficiency in aspirin resistance (AR) in patients with stable coronary artery disease (CAD) treated with aspirin. Material and methods: This study included 70 patients with stable CAD who had been using 100 mg aspirin for at least seven days. Serum 25-hydroxyvitamin D [25-(OH)D] concentration was measured and patients with 25-(OH)D level < 20 ng/dl were defined as the VD deficient group. A Multiplate Platelet Function Analyzer (Multiplate) device was used to evaluate AR. Patients were defined as aspirin-sensitive (AS) when their AUC was ≤ 30 U, and aspirin resistant (AR) when their AUC was > 30 U. Results: AUC was > 30 U in 15 (21%) patients and these patients were considered AR. The mean 25-(OH)D level was 18.7 ±12.2 ng/ml in all patients. Forty-five (64%) patients were VD deficient. The rate of AR was higher in the VD deficient group than the sufficient group (29% vs. 8%, p = 0.041). The mean AUC was higher in the VD deficient group than the sufficient group (30.2 ±29.1 vs. 15.3 ±13.1 U; p = 0.018). In ROC analysis 25-(OH)D level < 19.25 ng/dl predicted AR with 86.7% sensitivity, 61.8% specificity (AUC = 0.696, 95% CI: 0.551-0.840, p = 0.021). Conclusions: In the current study, an association was found between VD deficiency and AR in patients with stable CAD. VD supplementation may reduce platelet aggregation and overcome AR.
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A 59-year-old man who was admitted to the emergency department with new and spontaneous onset of fatigue, dyspnea, and palpitations. There was neither a history of trauma, chest pain, nor infection. Transthoracic two- and three-dimensional echocardiography and computer tomography demonstrated sinus of Valsalva aneurysm rupture dissecting interatrial septum and leading to a huge thrombus formation in it. The diagnosis with multimodality imaging performed within hours, and urgent surgery saved the patient's life.
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OBJECTIVE: Histologic plaque characteristics may influence the hemodynamic effect generated by physiologically significant unstable coronary lesions where plaque content and surface related factors are expected to contribute to the maximum translesional pressure drop. In this study, we aimed to identify local lesion specific virtual histological characteristics that may potentially affect hemodynamic outcome measures. METHODS: Forty-eight consecutive patients with non-ST-elevation acute coronary syndrome (NSTEACS) having paired hemodynamic and morphological data were enrolled. A dual sensor guide-wire was used for the assessment of fractional flow reserve (FFR) and stenosis resistance (HSR) in the culprit vessel. Virtual histology intravascular ultrasound imaging was performed after obtaining hemodynamic data. RESULTS: In a hemodynamically significant lesion subset (FFR<0.75 [n=34]), after controlling for lesion length, MLA and coronary artery compliance, FFR correlated with necrotic core (NC) area (r=-0.423, p=0.028) at MLA and NC volume (r=-0.497, p=0.008) and dense calcium (DC) volume (r=-0.332, p=0.03) across the entire lesion segment. Likewise, NC (r=-0.544, p=0.005) and DC (r=0.376, p=0.03) areas at MLA and NC (r=0.545, p=0.005) and DC (r=0.576, p=0.003) volumes across the entire lesion segment were associated with HSR in the hemodynamically significant lesion group (HSR>0.80 [n=33]). However, no correlation has been observed between intracoronary hemodynamic end-points and plaque components in hemodynamically insignificant lesions. CONCLUSIONS: This study demonstrated that for a given coronary stenosis geometry and arterial compliance, plaque composition may influence hemodynamic outcome measures in functionally significant stenoses in patients with NSTEACS.
