Impaired endothelium-dependent and endothelium-independent systemic vasodilatory reserve in pulmonary hypertension regardless the clinical group: A generalized dysfunction beyond the pulmonary arteries?

OBJECTIVE: Endothelium-dependent (ED) and endothelium-independent (EI) flow-mediated vasodilatation (FMD) have been used as measures of systemic arterial vasodilatory reserve. In this study, we aimed to assess both ED-FMD and EI-FMD in different groups with pulmonary hypertension (PH), and to investigate the relationship of these measures with clinical, echocardiographic, and invasive parameters of diseases severity and targeted treatment status. METHODS: Our study population comprised 41 patients with PH [28 (68.2%) women, age 46.3±19.6 years] including idiopathic pulmonary arterial hypertension, Eisenmenger syndrome, and chronic thromboembolic PH in whom diagnosis were confirmed in accordance with current guidelines and 17 age and sex-matched healthy controls. The brachial artery (BA) was used for assessment of FMD with Duplex ultrasound, and serial changes in diameter were recorded at baseline, 1, and 3 minutes after termination of 2-minute external occlusive compression for ED-FMD, and after sublingual intake of glycerol trinitrate for EI-FMD, respectively. RESULTS: Compared with controls, overall the PH group showed significantly lower ED-FMD (0.65±0.21 vs. 0.30±0.23 and 0.65±0.18 vs. 0.24±0.21) and EI-FMD (0.67±0.15 vs. 0.37±0.25 and 0.75±0.20 vs. 0.32±0.24) responses at 1st and 3rd min (p<0.001 for all). All these changes in the values of ED-FMD and EI-FMD were comparable among the PH subgroups. Neither ED-FMD nor EI-FMD were correlated with measures of PH severity and targeted therapy (TT) status (p>0.05). CONCLUSION: Our results suggest an impaired BA vasodilatory reserve in patients with PH regardless of the clinical subgroup. Although these findings seem to be consistent with systemic dysfunction, acute FMD may not reflect the severity of PH and cannot be used as a potential surrogate for outcome in this setting.

A new and simple method for clarifying the severity of tricuspid regurgitation.

BACKGROUND: No gold standard exists for grading tricuspid regurgitation (TR) severity. We developed a simple parameter, the right ventricular (RV) early inflow-outflow (RVEIO) index, using the early diastolic filling velocity and RV outflow velocity integrated over the systolic ejection period. We hypothesized that this index would help identify severe TR in clinical practice. METHODS: We obtained data from routine transthoracic echocardiograms. All records reporting moderate (n=395) or severe (n=395) TR were reanalyzed to measure vena contracta (VC) width, TR jet area, effective regurgitant orifice (EROA) derived with the proximal isovelocity surface area method, RVEIO index, and right-sided chamber volumes. RESULTS: Significant linear trends were demonstrated for right atrial volume index, end-diastolic volume index, E-wave velocity, RV velocity time integral, TR jet area, VC width, and EROA with increasing TR severity. Independent predictors of severe RT included RVEIO index ≥ 10, VC width ≥ 0.7 cm, TR jet area>10 cm2 , and EROA ≥ 0.4 cm2 . CONCLUSION: RVEIO index is a useful, simple, accurate, and independent predictor of severe TR that adds incrementally to traditional methods of quantifying TR severity. Accurate quantification and classification of TR severity is critical for clinical decision-making and management; therefore, the incorporation of RVEIO index into the integrative approach to grading TR severity should be considered.

Platelet/lymphocyte ratio was associated with impaired myocardial perfusion and both in-hospital and long-term adverse outcome in patients with ST-segment elevation acute myocardial infarction undergoing primary coronary intervention.

INTRODUCTION: Platelet/lymphocyte ratio (PLR) has been shown to be an inflammatory and thrombotic biomarker for coronary heart disease, but its prognostic value in ST-segment elevation myocardial infarction (STEMI) has not been fully investigated. AIM: To investigate the relationship between PLR and no-reflow, along with the in-hospital and long-term outcomes in patients with STEMI. MATERIAL AND METHODS: In the present study, we included 304 consecutive patients suffering from STEMI who underwent primary percutaneous coronary intervention (p-PCI). Patients were stratified according to PLR tertiles based on the blood samples obtained in the emergency room upon admission. No-reflow after p-PCI was defined as a coronary thrombolysis in myocardial infarction (TIMI) flow grade ≤ 2 after vessel recanalization, or TIMI flow grade 3 together with a final myocardial blush grade (MBG) < 2. RESULTS: The mean follow-up period was 24 months (range: 22-26 months). The number of patients characterized with no-reflow was counted to depict increments throughout successive PLR tertiles (14% vs. 20% vs. 45%, p < 0.001). In-hospital major adverse cardiovascular events and death increased as the PLR increased (p < 0.001, p < 0.001). Long-term MACE and death also increased as the PLR increased (p < 0.001, p < 0.001). Multivariable logistic regression analysis revealed that PLR remained an independent predictor for both in-hospital (OR = 1.01, 95% CI: 1.00-1.01; p = 0.002) and major long-term (OR = 1.01, 95% CI: 1.00-1.01; p < 0.001) adverse cardiac events. CONCLUSIONS: Platelet/lymphocyte ratio on admission is a strong and independent predictor of both the no-reflow phenomenon and long-term prognosis following p-PCI in patients with STEMI.

Coronary Subclavian Steal Syndrome Evaluated with Multimodality Imaging.

In patients with mammary-coronary bypass grafts, the presence of a subclavian artery stenosis proximal to the internal mammary artery may result in a condition termed coronary-subclavian steal syndrome of which the incidence varies between 0.07-3.4% among those requiring coronary grafts. We reported a patient with a history of the coronary artery bypass graft who presented with typical angina pectoris at rest that was exacerbated by selective exercise of the left upper extremity in whom occlusion of the left subclavian artery was demonstrated in this patient by 3D reconstruction of computed tomography angiography, a reversal blood flow in the left internal mammary artery-left anterior descending artery graft by Doppler ultrasonography, and a coronary angiography.