Coronary microcirculation in nonculprit vessel territory in reperfused acute myocardial infarction.

BACKGROUND: There is an ongoing debate on the extension of reperfusion-related microvascular damage (MVD) throughout the remote noninfarcted myocardial regions in patients with ST-elevation myocardial infarction (STEMI) that undergo primary percutaneous intervention (pPCI). The aim of this study was to elucidate the impact of reperfusion on remote microcirculatory territory by analyzing hemodynamic alterations in the nonculprit-vessel in relation to reperfusion. METHODS: A total of 20 patients with STEMI undergoing pPCI were included. Peri-reperfusion temporal changes in hemodynamic parameters were obtained in angiographically normal nonculprit vessels before and 1-h after reopening of the culprit vessel. Intracoronary pressure and flow velocity data were compared using pairwise analyses (before and 1-h after reperfusion). RESULTS: In the non-culprit vessel, compared to the pre-reperfusion state, mean resting average peak velocity (33.4 ± 9.4 to 25.0 ± 4.9 cm/s, P < 0.001) and mean hyperemic average peak velocity (53.5 ± 14.4 to 42.1 ± 10.66 cm/s, P = 0.001) significantly decreased; whereas baseline (3.2 ± 1.0 to 4.0 ± 1.0 mmHg.cm-1.s, P < 0.001) and hyperemic microvascular resistance (HMR) (1.9 ± 0.6 to 2.4 ± 0.7 mmHg.cm-1.s, P < 0.001) and mean zero flow pressure (Pzf) values (32.5 ± 6.9 to 37.6 ± 8.3 mmHg, P = 0.003) significantly increased 1-h after reperfusion. In particular, the magnitude of changes in HMR and Pzf values following reperfusion were more prominent in patients with larger infarct size and with higher extent of MVD in the culprit vessel territory. CONCLUSION: Reperfusion-related microvascular injury extends to involve remote myocardial territory in relation to the magnitude of the adjacent infarction and infarct-zone MVD. (GUARD Clinical TrialsNCT02732080).

Galectin-3 as a Novel Biomarker for Predicting Clinical Outcomes in Hospitalized COVID-19 Patients.

BACKGROUND: Galectin-3 has been shown to play a key pathophysiological role in pulmonary associated inflammatory response and lung fibrosis in COVID-19 and is a mediator for viral adhesion. However, there is limited data about its potential role in severity and prognosis of COVID-19. This study aimed to investigate the predictive role of serum galectin-3 concentrations in the severe clinical outcomes of hospitalized COVID-19 patients: the severity of pneumonia, in-hospital mortality, and the need for intensive care unit (ICU) admission. METHODS: This single-center study included 68 patients with laboratory- and radiologically-confirmed COVID-19 admitted to our emergency department. The study population was divided into patients with primary clinical out-comes (n = 32) and those without (n = 36). The need for ICU admission and/or in-hospital mortality were the primary clinical endpoints. The study group was also classified based on pneumonia severity: severe or mild/moderate. Blood samples were collected within 48 hours of admission to estimate serum galectin-3 concentrations. RESULTS: Multivariate regression analysis showed that lower concentrations of galectin-3 and arterial oxygen saturation (SpO2) were independently associated with the primary clinical outcomes (OR = 0.951, p = 0.035; OR = 0.862, p = 0.017, respectively); increased concentrations of galectin-3 were an independent predictor of severe pneumonia (OR = 1.087, p = 0.016). In the receiver operating characteristics curve analysis, serum galectin-3 concentrations at hospital admission predicted pneumonia severity with 52.1% sensitivity and 90% specificity with a cutoff of 38.76 ng/mL. CONCLUSIONS: Circulating galectin-3 at hospital admission could be a useful biomarker for identifying COVID-19 patients at high risk for severe pneumonia.

The relation of echo-derived lateral MAPSE to left heart functions and biochemical markers in patients with preserved ejection fraction: Short-term prognostic implications.

OBJECTIVE: Mitral annular plane systolic excursion (MAPSE) is a simple way to evaluate-left ventricle (LV) function. Our aim was to explain the relationship of MAPSE with LV function and biochemical markers in patients with preserved ejection fraction (EF), and to determine whether it has an effect on prognosis in echocardiography (echo) practice. METHODS: Consecutive patients referred to the echo laboratory between November 2020 and March 2021 were included in the study. In addition to conventional parameters, MAPSE of the lateral mitral annulus was measured in all patients. Patients were divided into three groups according to lateral MAPSE: low (<12 mm), relatively preserved (12-15 mm), and high (≥15 mm). RESULTS: A total of 512 patients with preserved EF were included in the study. MAPSE was low in 44 patients (9%), relatively preserved in 231 patients (45%), and high in 237 patients (46%). The mean age was higher in the low group compared to the other two groups (p < 0.001) and the body mass index was increased in the low group compared to the high group (p = 0.010). Atrial fibrillation and hypertension were more common in patients with low MAPSE. The rate of diastolic dysfunction (DD) and all-cause hospitalization were higher in the low and relatively preserved groups than in the high group (p < 0.001, p = 0.002; respectively). The pro-BNP level and mortality rate were higher in the low group compared to the relatively preserved and high groups (p = 0.007, p = 0.005; respectively). MAPSE was identified as independent predictor of hospitalization (OR: 0.284, 95% CI: 0.093-0.862, p = 0.026) via multivariate analysis and independent predictor of in-hospital mortality (HR: 0.002, 95% CI: 0-0.207, p = 0.008). CONCLUSIONS: Analysis of LV longitudinal function by echo-derived lateral MAPSE when LV ejection fraction is normal provides important information about DD and related heart failure and may predict prognosis in echo practice.

The Interplay between Features of Plaque Vulnerability and Hemodynamic Relevance of Coronary Artery Stenoses.

Fractional flow reserve (FFR) may not be immune from hemodynamic perturbations caused by both vessel and lesion related factors. The aim of this study was to investigate the impact of plaque- and vessel wall-related features of vulnerability on the hemodynamic effect of intermediate coronary stenoses. Methods and Results: In this cross-sectional study, patients referred to catheterization laboratory for clinically indicated coronary angiography were prospectively screened for angiographically intermediate stenosis (50-80%). Seventy lesions from 60 patients were evaluated. Mean angiographic stenosis was 62.1 ± 16.3%. After having performed FFR assessment, intravascular ultrasound (IVUS) was performed over the FFR wire. Virtual histology IVUS was used to identify the plaque components and thin cap fibroatheroma (TCFA). TCFA was significantly more frequent (65 vs. 38%, p = 0.026), and necrotic core volume (26.15 ± 14.22 vs. 16.21 ± 8.93 mm3, p = 0.04) was significantly larger in the positively remodeled than non-remodeled vessels. Remodeling index correlated with necrotic core volume (r = 0.396, p = 0.001) and with FFR (r = -0. 419, p = 0.001). With respect to plaque components, only necrotic core area (r = -0.262, p = 0.038) and necrotic core volume (r = -0.272, p = 0.024) were independently associated with FFR. In the multivariable model, presence of TCFA was independently associated with significantly lower mean FFR value as compared to absence of TCFA (adjusted, 0.71 vs. 0.78, p = 0.034). Conclusion: The current study demonstrated that for a given stenosis geometry, features of plaque vulnerability such as necrotic core volume, TCFA, and positive remodeling may influence the hemodynamic relevance of intermediate coronary stenoses.

Endocan: a novel biomarker associated with well-developed coronary collateral circulation in patients with stable angina and chronic total occlusion.

Angiogenesis and arteriogenesis have a crucial role in the formation of coronary collateral vessels. It has been shown that endocan and vascular cell adhesion molecule-1 (VCAM-1) are potential angiogenetic factors. We investigated the relationship between serum endocan levels and grade of coronary collaterals, and also the correlation of endocan levels with serum VCAM-1 levels. Patients with stable angina and at least one total coronary occlusion at invasive coronary angiography were included in our study. Collateral degree was graded according to Rentrop and Cohen's classification. Patients who had grade 0 or 1 collateral vessels were included in the poorly-developed collateral group, and those with grade 2 or 3 coronary collateral vessels were included in the well-developed collateral group. Serum endocan and VCAM-1 levels were significantly higher in the well-developed collateral group (436.6 ± 213.3 ng/mL vs. 216.1 ± 78.5 ng/mL, p < .001; 11.02 ± 6.58 ng/mL vs. 6.78 ± 1.14 ng/mL, p < .001, respectively). In a logistic regression analysis, only serum endocan level remained as an independent predictor for good collateral development. In the ROC curve analysis, 282 ng/mL endocan level had an a 82 % sensitivity and 86 % specificity for prediction of the well-developed collateral group. Higher endocan level was related to better coronary collateral development. In the event that these results are confirmed in further studies, endocan may be considered as an anti-ischemic treatment strategy in order to improve collateral development.

A Mysterious Crescent in the Heart: Ruptured Sinus of Valsalva Dissecting Interatrial Septum, Multimodality Imaging, and Full Recovery.

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.

Identification of gene variants associated with hypoxia pathway in acute coronary syndrome: a pilot study.

Hypoxic condition is known to play an important role in the development of acute coronary syndrome (ACS) and understanding mechanism of hypoxic effects is essential to develop new treatment strategies for ACS. Based on the phenotypic features of cardiovascular diseases, it is claimed that genetic factors play an important role in the development genome-wide association studies have been studied to clarify the molecular mechanisms underlying heritable and prevalent phenotype. The claim was to investigate possible roles of gene polymorphisms involving in hypoxia pathway on ACS in this pilot study. DNA samples of 100 ACS cases and 100 controls from a Department of Cardiology, Istanbul University, were genotyped with Illumina CytoSNP-12 BeadChip 300 K Array. The additive model used for statistical analysis, and Correlation/Trend Test selected as a statistical process. It was determined different criteria for association analysis as case/control and number of plugged vessels. P value calculated with each SNP and score generated with -log10(P). Also, hypoxia pathway analysis was applied to find statistically significant genes. As a result of bioinformatic analysis, it was claimed that PIAS4 (rs735842) and VEGFA (rs699947) were the most statistically significant variants associated in hypoxia pathway analysis. Due to the information of literature, there have been no prior studies of possible interactions of hypoxia pathways the etiology of acute coroner syndromes in the same research. Detailed studies with larger sample groups are necessary to clarify the role of hypoxia in the development of disease.

Gradual Versus Abrupt Reperfusion During Primary Percutaneous Coronary Interventions in ST-Segment-Elevation Myocardial Infarction (GUARD).

Background Intramyocardial edema and hemorrhage are key pathological mechanisms in the development of reperfusion-related microvascular damage in ST-segment-elevation myocardial infarction. These processes may be facilitated by abrupt restoration of intracoronary pressure and flow triggered by primary percutaneous coronary intervention. We investigated whether pressure-controlled reperfusion via gradual reopening of the infarct-related artery may limit microvascular injury in patients undergoing primary percutaneous coronary intervention. Methods and Results A total of 83 patients with ST-segment-elevation myocardial infarction were assessed for eligibility and 53 who did not meet inclusion criteria were excluded. The remaining 30 patients with totally occluded infarct-related artery were randomized to the pressure-controlled reperfusion with delayed stenting (PCRDS) group (n=15) or standard primary percutaneous coronary intervention with immediate stenting (IS) group (n=15) (intention-to-treat population). Data from 5 patients in each arm were unsuitable to be included in the final analysis. Finally, 20 patients undergoing primary percutaneous coronary intervention who were randomly assigned to either IS (n=10) or PCRDS (n=10) were included. In the PCRDS arm, a 1.5-mm balloon was used to achieve initial reperfusion with thrombolysis in myocardial infarction grade 3 flow and, subsequently, to control distal intracoronary pressure over a 30-minute monitoring period (MP) until stenting was performed. In both study groups, continuous assessment of coronary hemodynamics with intracoronary pressure and Doppler flow velocity was performed, with a final measurement of zero flow pressure (primary end point of the study) at the end of a 60-minute MP. There were no complications associated with IS or PCRDS. PCRDS effectively led to lower distal intracoronary pressures than IS over 30 minutes after reperfusion (71.2±9.37 mm Hg versus 90.13±12.09 mm Hg, P=0.001). Significant differences were noted between study arms in the microcirculatory response over MP. Microvascular perfusion progressively deteriorated in the IS group and at the end of MP, and hyperemic microvascular resistance was significantly higher in the IS arm as compared with the PCDRS arm (2.83±0.56 mm Hg.s.cm-1 versus 1.83±0.53 mm Hg.s.cm-1, P=0.001). The primary end point (zero flow pressure) was significantly lower in the PCRDS group than in the IS group (41.46±17.85 mm Hg versus 76.87±21.34 mm Hg, P=0.001). In the whole study group (n=20), reperfusion pressures measured at predefined stages in the early reperfusion period showed robust associations with zero flow pressure values measured at the end of the 1-hour MP (immediately after reperfusion: r=0.782, P<0.001; at the 10th minute: r=0.796, P<0.001; and at the 20th minute: r=0.702, P=0.001) and peak creatine kinase MB level (immediately after reperfusion: r=0.653, P=0.002; at the 10th minute: r=0.597, P=0.007; and at the 20th minute: r=0.538, P=0.017). Enzymatic myocardial infarction size was lower in the PCRDS group than in the IS group with peak troponin T (5395±2991 ng/mL versus 8874±1927 ng/mL, P=0.006) and creatine kinase MB (163.6±93.4 IU/L versus 542.2±227.4 IU/L, P<0.001). Conclusions In patients with ST-segment-elevation myocardial infarction, pressure-controlled reperfusion of the culprit vessel by means of gradual reopening of the occluded infarct-related artery (PCRDS) led to better-preserved coronary microvascular integrity and smaller myocardial infarction size, without an increase in procedural complications, compared with IS. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02732080.

Intracardiac masses: Single center experience within 12 years: I-MASS Study.

Objective: The aim of this cross-sectional, retrospective, descriptive study was to review and classify cardiac masses systematically and to determine their frequencies. Methods: The medical records of 64,862 consecutive patients were investigated within 12 years. Every patient with a cardiac mass imaged by transthoracic echocardiography (TTE) and confirmed with an advanced imaging modality such as transesophageal echocardiography (TEE), computed tomography (CT) and/or cardiac magnetic resonance imaging (CMR) was included. Acute coronary syndromes triggering thrombus formation, vegetations, intracardiac device and catheter related thrombi were excluded. Results: Data demonstrated 127 (0.195%) intracardiac masses consisting of 33 (0.050%) primary benign, 3 (0.004%) primary malignant, 20 (0.030%) secondary tumors, 3 (0.004%) hydatid cysts and 68 (0.104%) thrombi respectively. The majority of primary cardiac tumors were benign (91.67%), predominantly myxomas (78.79%), and the less malignant (8.33%). Secondary cardiac tumors were common than the primary malignant tumors (20:3), with male dominancy (55%), lymphoma and lung cancers were the most frequent. Intracardiac thrombi was the majority of the cardiac masses, thrombi accompanying malignancies were in the first range (n = 17, 25%), followed by autoimmune diseases (n = 13, 19.12%) and ischemic heart disease with low ejection fraction (n = 12, 17.65%). Conclusions: This retrospective analysis identified 127 patients with cardiac masses. The majority of benign tumors were myxoma, the most common tumors that metastasized to the heart were lymphoma and lung cancers, and the thrombi associated with malignancies and autoimmune diseases were the most frequent.

High concentrations of asymmetric dimethylarginine are associated with ST-segment resolution failure after reperfusion for acute myocardial infarction.

BACKGROUND: Increased concentrations of asymmetric dimethylarginine (ADMA) have been detected in patients with cardiovascular risk factors. In addition, high baseline plasma concentrations of ADMA have been shown to be an independent predictor of adverse outcomes in various disorders. This study aimed to evaluate the impact of admission ADMA concentrations on microvascular flow after primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: Blood samples from 39 patients with STEMI were collected at admission to measure the concentrations of ADMA and other cardiovascular risk factors including inflammatory markers and the lipid profile. Primary PCI was performed in patients with STEMI. The maximum ST-segment elevation in standard 12-leads electrocardiogram (ECG) before and 24 h after PCI was measured, and patients were stratified as complete or incomplete ST-segment resolution (STR). RESULTS: Twenty-five patients had complete (≥ 70%) and 14 incomplete (<70%) STR. In patients with incomplete STR, ADMA concentrations were significantly higher than that seen in others (0.447 ± 0.215 µmol/L vs. 0.310 ± 0.134, p=0.019), and was independently associated with STR. CONCLUSIONS: Admission concentrations of ADMA appeared to be useful for early risk stratification in reperfusion therapy for acute myocardial infarction.

True left ventricular aneurysm after blunt chest trauma.

Left ventricular aneurysms are common in clinical practice. Although their underlying aetiology is generally clear by the clinical context, it can be hard to define the exact cause in some cases. We report a case of a patient in whom cardiac MRI provided important information about the differential diagnosis of a left ventricular aneurysm.

Impairment of right ventricular longitudinal strain associated with severity of pneumonia in patients recovered from COVID-19.

Myocardial injury caused by COVID-19 was reported in hospitalized patients previously. But the information about cardiac consequences of COVID-19 after recovery is limited. The aim of the study was comprehensive echocardiography assessment of right ventricular (RV) in patients recovered from COVID-19. This is a prospective, single-center study. After recovery from COVID-19, echocardiography was performed in consecutive 79 patients that attended follow-up visits from July 15 to November 30, 2020. According to the recovery at home vs hospital, patients were divided into two groups: home recovery (n = 43) and hospital recovery (n = 36). Comparisons were made with age, sex and risk factor-matched control group (n = 41). In addition to conventional echocardiography parameters, RV global longitudinal strain (RV-GLS) and RV free wall strain (RV-FWS) were determined using 2D speckle-tracking echocardiography (2D STE). Of the 79 patients recovered from COVID-19, 43 (55%) recovered at home, while 36 (45%) required hospitalization. The median follow-up duration was 133  ±  35 (87-184) days. In patients recovered from hospital, RV-GLS and RV-FWS were impaired compared to control group (RV-GLS: -17.3  ±  6.8 vs. -20.4  ±  4.9, respectively [p = 0.042]; RV-FWS: -19.0  ±  8.2 vs. -23.4  ±  6.2, respectively [p = 0.022]). In subgroup analysis, RV-FWS was impaired in patients severe pneumonia (n = 11) compared to mild-moderate pneumonia (n = 28), without pneumonia (n = 40) and control groups (-15.8  ±  7.6 vs. -21.6  ±  7.6 vs. -20.8  ±  7.7 vs. -23.4  ±  6.2, respectively, [p = 0.001 for each]) and RV-GLS was impaired compared to control group (-15.2  ±  6.9 vs. -20.4  ±  4; respectively, [p = 0.013]). A significant correlation was detected between serum CRP level at hospital admission and both RV-GLS and RV-FWS (r = 0.285, p = 0.006; r = 0.294, p = 0.004, respectively). Age (OR 0.948, p = 0.010), male gender (OR 0.289, p = 0.009), pneumonia on CT (OR 0.019, p = 0.004), and need of steroid in treatment (OR 17.424, p = 0.038) were identifed as independent predictors of impaired RV-FWS (> -18) via multivariate analysis. We demonstrated subclinic dysfunction of RV by 2D-STE in hospitalized patients in relation to the severity of pneumonia after recovery from COVID-19. 2D-STE supplies additional information above standard measures of RV in this cohort and can be used in the follow-up of these patients.

Evaluation the relationship of left ventricular global longitudinal strain and laboratory parameters in discharged patients with COVID-19: a follow-up study.

BACKGROUND: The novel coronavirus infection (COVID-19) disease has spread rapidly and posed a great threat to global public health. The laboratory parameters and clinical outcomes of the disease in discharged patients remain unknown. In this study, we aimed to investigate the laboratory and echocardiographic findings of patients with COVID-19 after discharge and the relation between left ventricular global longitudinal strain (LVGLS) and inflammatory parameters in discharged patients. METHODS: A total of 75 patients recovering from COVID-19 as the study group were prospectively recruited from the COVID-19 outpatient clinic for their follow-up visits at a median 6 months after discharge. Patients were classified into groups according to pneumonia severity and impairment in LVGLS. Laboratory findings of patients both at admission and after discharge were evaluated and the relation with pneumonia severity at admission and LVGLS after discharge were analyzed. RESULTS: Serum ferritin, lactate dehydrogenase (LDH) and prohormone B-type natriuretic peptide (pro-BNP) levels after discharge were significantly higher in the study group than the control group (n = 44). Ferritin was found to be related to pneumonia severity. Serum ferritin and LDH values after discharge were significantly higher in patients with impaired LVGLS than those with preserved. There was a significant correlation between LVGLS, serum ferritin and LDH values after discharge (r = -0.252, p = 0.012; r = -0.268, p = 0.005, respectively). CONCLUSIONS: Clinicians should pay close attention to the serum ferritin and LDH levels in discharged patients for predicting the severity of COVID-19 disease and early identification of subclinical left ventricular myocardial dysfunction.

Role of global longitudinal strain in discriminating variant forms of left ventricular hypertrophy and predicting mortality.

OBJECTIVE: In this study, we aimed to compare the functional adaptations of the left ventricle in variant forms of left ventricular hypertrophy (LVH) and to evaluate the use of two-dimensional speckle tracking echocardiography (2D-STE) in differential diagnosis and prognosis. METHODS: This was a prospective cohort study of 68 patients with LVH, including 20 patients with non-obstructive hypertrophic cardiomyopathy (HCM), 23 competitive top-level athletes free of cardiovascular disease, and 25 patients with hypertensive heart disease (HHD). All the subjects underwent 2D transthoracic echocardiography (TTE) and 2D-STE. The primary endpoint was all-cause mortality. Global longitudinal strain (GLS) below -12.5% was defined as severely reduced strain, -12.5% to -17.9% as mildly reduced strain, and above -18% as normal strain. RESULTS: The mean LV-GLS value was higher in athletes than in patients with HCM and HHD with the lowest value being in the HCM group (HCM: -11.4±2.2%; HHD: -13.6±2.6%; and athletes: -15.5±2.1%; p<0.001 among groups). LV-GLS below -12.5% distinguished HCM from others with 65% sensitivity and 77% specificity [area under curve (AUC)=0.808, 95% confidence interval (CI): 0.699-0.917, p<0.001]. The median follow-up duration was 6.4±1.1 years. Overall, 11 patients (16%) died. Seven of these were in the HHD group, and four were in the HCM group. The mean GLS value in patients who died was -11.8±1.5%. LV-GLS was significantly associated with mortality after adjusting age and sex via multiple analysis (RR=0.723, 95% CI: 0.537-0.974, p=0.033). Patients with GLS below -12.5% had a higher risk of all-cause mortality compared with that of patients with GLS above -12.5% according to Kaplan-Meier survival analysis for 7 years (29% vs. 9%; p=0.032). The LV-GLS value predicts mortality with 64% sensitivity and 70% specificity with a cut-off value of -12.5 (AUC=0.740, 95% CI: 0.617-0.863, p=0.012). CONCLUSION: The 2D-STE provides important information about the longitudinal systolic function of the myocardium. It may enable differentiation variable forms of LVH and predict prognosis.

Intracoronary streptokinase after primary percutaneous coronary intervention.

BACKGROUND: Microvascular perfusion is often impaired after primary percutaneous coronary intervention (PCI). We proposed that in situ thrombosis might contribute to poor myocardial perfusion in this setting. To test this hypothesis, we evaluated the effect of low-dose intracoronary streptokinase administered immediately after primary PCI. METHODS: Forty-one patients undergoing primary PCI were randomly assigned to receive intracoronary streptokinase (250 kU) or no additional therapy. Two days later, cardiac catheterization was repeated, and coronary hemodynamic end points were measured with the use of a guidewire tipped with pressure and temperature sensors. In patients with anterior myocardial infarction, the deceleration time of coronary diastolic flow was measured with transthoracic echocardiography. At 6 months, angiography, echocardiography, and technetium-99m single-photon-emission computed tomography were performed. RESULTS: Two days after PCI, all measures of microvascular function (means +/-SD) were significantly better in the streptokinase group than in the control group, including coronary flow reserve (2.01+/-0.57 vs. 1.39+/-0.31), the index of microvascular resistance (16.29+/-5.06 U vs. 32.49+/-11.04 U), the collateral-flow index (0.08+/-0.05 vs. 0.17+/-0.07), mean coronary wedge pressure (10.81+/-5.46 mm Hg vs. 17.20+/-7.93 mm Hg), systolic coronary wedge pressure (18.24+/-6.07 mm Hg vs. 33.80+/-11.00 mm Hg), and diastolic deceleration time (828+/-258 msec vs. 360+/-292 msec). The administration of intracoronary streptokinase was also associated with a significantly lower corrected Thrombolysis in Myocardial Infarction frame count (the number of cine frames required for dye to travel from the ostium of a coronary artery to a standardized distal coronary landmark) at 2 days. At 6 months, however, there was no evidence of a difference between the two study groups in left ventricular size or function. CONCLUSIONS: In our pilot trial, the administration of low-dose intracoronary streptokinase immediately after primary PCI improved myocardial reperfusion but not long-term left ventricular size or function. These findings require clarification in a larger trial. (ClinicalTrials.gov number, NCT00302419.)

Influences of genetic variants in interleukin-15 gene and serum interleukin-15 levels on coronary heart disease.

Interleukin-15 (IL-15) is a potent proinflammatory cytokine that is now considered a key component of atherosclerosis. Proinflammatory gene polymorphisms lead to variations in the production and level of the proteins. In light of these findings, we hypothesized that variations in the gene coding for IL-15 influence the risk of coronary heart disease (CHD) by modulating the IL-15 levels. To test this hypothesis, we examined 5 single nucleotide polymorphisms (SNPs) in IL-15 gene and IL-15 levels in 102 patients with acute coronary syndrome (ACS), 102 patients with chronic ischemic stable CHD and 162 healthy control subjects. This study is the first report showing the influences of IL-15 gene variants and IL-15 levels on CHD. The five single nucleotide polymorphisms (SNPs) within the IL-15 gene, G367A, C267T, A14035T, C13687A, and A10504G were carried out by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). Serum IL-15 levels were significantly higher in both acute and chronic patients than in controls. Genetic variants of IL-15 gene and IL-15 levels were associated with CHD. In conclusion, our study supports the hypothesis that genetic variation in IL-15 gene and IL-15 levels influence the risk of CHD. Further studies are needed to confirm our hypothesis.

Homocysteine and pro-inflammatory cytokine concentrations in acute heart disease.

Inflammation is involved in development and progression of atherosclerosis. Interleukin-2 (IL-2) and interleukin-6 (IL-6) have been correlated with various cardiovascular diseases. Hyperhomocysteinemia is an important risk factor for atherosclerosis and thrombotic disease. Recent studies have demonstrated that homocysteine (Hcy) enhances productions of several pro-inflammatory cytokines. In the light of these findings, we decided to determine if any relationship exists between IL-2 and IL-6, the pro-inflammatory cytokines, and total homocysteine (tHcy) in acute coronary syndrome (ACS). A total of 102 patients with ACS and 90 healthy subjects were included in the study. The levels of tHcy, IL-2 and IL-6 were higher and folic acid was lower in patients as compared with those of controls. Furthermore, data of the area under ROC plot for IL-2 demonstrated that IL-2 had higher sensitivity. These data suggest that enhanced inflammation may be associated with tHcy-related cardiovascular disease.

The accuracy of deceleration time of diastolic coronary flow measured by transthoracic echocardiography in predicting long-term left ventricular infarct size and function after reperfused myocardial infarction.

AIMS: Assessment of microvascular function after reperfused acute myocardial infarction (AMI) provides important insights for myocardial reperfusion and facilitates prediction of long-term left ventricular (LV) function and clinical outcome. In this study, we examined microvascular integrity 48 h after successful primary percutaneous coronary intervention (PCI) and compared predictive accuracy of the intracoronary pressure-wire- and transthoracic Doppler echocardiography-based parameters in the estimation of long-term LV infarct size and function. METHODS AND RESULTS: The study group consisted of 30 anterior AMI patients who were treated successfully with primary PCI. Two days after primary PCI, microvascular integrity was evaluated. Coronary flow reserve (CFR), collateral flow index (CFIp), coronary wedge pressure (CWP), and index of microvascular resistance (IMR) were determined using intracoronary pressure wire. Deceleration time of coronary diastolic flow (DDT) was measured using transthoracic echocardiography. At 6 months, coronary angiography, echocardiography, and infarct size measurement were performed. Area under the curve, sensitivity, and specificity of the indices of microvascular perfusion in the prediction of late-term infarct size were as follows: IMR (0.68 ± 0.15, 69%, 60%), CFR (0.67 ± 0.10, 66%, 59%), CWP (0.69 ± 0.12, 70%, 72%), CFIp (0.64 ± 0.10, 65%, 78%), and DDT (0.68 ± 0.16, 69%, 79%). All of the microvascular perfusion indices, which have been used in this study, had comparable sensitivity and specificity in the prediction of long-term ejection fraction. There were no significant differences between areas under the curve of microvascular perfusion indices in the prediction of long-term infarct size and ejection fraction. CONCLUSION: As a non-invasive parameter, DDT was found to be as accurate as the invasive parameters of microvascular function in estimating long-term infarct size and LV function. Thus, simply measuring DDT in the reperfused infarct-related artery might provide useful and reliable estimate for early risk stratification.

Impact of myocardial acceleration during isovolumic contraction in evaluating subclinical right ventricular systolic dysfunction in type 2 diabetes mellitus patients.

AIM: In diabetes mellitus (DM) patients, left ventricular dysfunction is widely evaluated and established by conventional diagnostic methods, whereas right ventricular (RV) function is not as sufficiently evaluated. The aim of this study is to assess the preclinical effects of DM on RV function by using novel Tissue Doppler Imaging (TDI)-derived indices. METHODS: The study included 96 patients with type II DM [60 with DM only and 36 patients with coexisting DM and hypertension (DMHT)] and 40 healthy controls. Conventional parameters and TDI-derived systolic velocities of tricuspid annulus [isovolumic myocardial acceleration (IVA), peak myocardial velocity during isovolumic contraction (IVV), peak systolic velocity during ejection period (Sa), RV Tei index] were measured. RESULTS: TDI-derived RV IVA was significantly lower in both DM and DMHT patients compared to controls indicating subclinical impairment in RV systolic function in the study patients (P = 0,0001). However RV IVA was similar in DM and DMHT subgroup supporting RV systolic impairment in DM was independent from HT. In correlation analysis, RV IVA was significantly correlated with the existence of diabetic nephropathy (r =-0,38; P = 0,003), retinopathy (r =-0,35; P = 0,006), insulin resistance (r =-0,52; P = 0,0001). CONCLUSIONS: Diabetes is associated with subclinical RV systolic dysfunction, regardless of coexisting hypertension. Tissue Doppler-derived IVA; is a novel, non-invasive parameter which may be used in early detection of RV systolic dysfunction in patients with DM.