Piotr Klimeczek

Extent of RV Dysfunction and Myocardial Infarction Assessed by CMR Are Independent Outcome Predictors Early After STEMI Treated With Primary Angioplasty

OBJECTIVES The aim of this study was to assess the prognostic value of right ventricular (RV) involvement diagnosed by cardiac magnetic resonance (CMR) early after ST-elevation myocardial infarction (STEMI). BACKGROUND CMR allows accurate and reproducible RV assessment. However, there is a paucity of data regarding the prognostic value of RV involvement detected by CMR early after STEMI. METHODS Ninety-nine patients (77 men, mean age 57 ± 11 years) who underwent CMR 3 to 5 days after STEMI treated with primary angioplasty were followed for 1,150 ± 337 days for cardiac events (cardiac death, nonfatal myocardial infarction [MI], and hospitalizations due to decompensated heart failure). Cox proportional hazards model was applied in stepwise forward fashion to identify outcome predictors. Event-free survival was estimated by Kaplan-Meier method and compared between groups by the log-rank test. RESULTS Cardiac events occurred in 34 patients (7 cardiac deaths, 8 MIs, 26 hospitalizations). By multivariable analysis, the independent outcome predictors were left ventricular (LV) MI transmurality index (hazard ratio: 1.03 per 1%; 95% confidence interval: 1.01 to 1.04; p = 0.001), RV ejection fraction (RVEF) (hazard ratio: 1.46 per 10% decrease; 95% confidence interval: 1.05 to 2.02; p = 0.03), and RVMI extent (hazard ratio: 1.50 per each infarcted RV segment; 95% confidence interval: 1.11 to 2.01; p = 0.007). Compared with clinical data (global chi-square = 5.2), LV ejection fraction [LVEF] (global chi-square = 11.1), RVEF (global chi-square = 17.1), LVMI transmural extent (global chi-square = 26.0), and RVMI extent (global chi-square = 34.9) improved outcome prediction in sequential Cox model analysis (p < 0.05 for all steps). RVEF stratified risk in patients with LVEF <40% in whom the 4-year event-free survival was 66.7% for RVEF ≥40% and 40.0% for RVEF <40% (p < 0.05). CONCLUSIONS The extent of RVMI and RV dysfunction assessed early after STEMI are independent outcome predictors, which provide incremental prognostic value to clinical data, LV systolic function, and infarct burden. Measurement of RVEF may be particularly useful to stratify risk in patients with depressed LV function after STEMI.

Physical training in patients with chronic heart failure of ischemic origin: effect on exercise capacity and left ventricular remodeling:

Background Physical training is a well-known complementary treatment for chronic heart failure (CHF); however, many aspects require further studies. One of them is the impact on remodeling of the left ventricle (LV). The purpose of this study was to evaluate the effect of 6 months of training on LV, exercise capacity and safety issues in patients with ischemic CHF. Methods Fifty patients (mean age 60.1 ± 9.2 years) with ischemic CHF, New York Heart Association (NYHA) classification class II and III and left ventricular ejection fraction (LVEF) ≤ 35% were randomized into groups: undergoing 6-month training (25 patients) and not trained (25 patients). In both groups at baseline and at 6 months a cardiopulmonary exercise test and magnetic resonance imaging (MRI) with evaluation of LV were performed. Training was limited by the achievement of 80% of the predicted heart rate at VO2PEAK achieved at the baseline cardiopulmonary exercise test. Results All patients completed the 6-month observation. No serious adverse events were found in either group. Exercise capacity improved only in the trained group (VO 2peak increased by 31%). At 6 months in the trained group there was a tendency towards an improvement in some LV parameters: ejection fraction, end-diastolic volume and wall motion score index (WMSI), whereas an opposite trend was seen in the controls (P < 0.05, P < 0.05 and P < 0.01 for comparison of LVEFs, end-diastolic volumes and WMSIs, respectively). Conclusions Six-month training in ischemic CHF patients is a safe modality. Training improves exercise capacity. There was no negative impact on LV morphology, and a trend towards improvement of functional parameters on MRI may suggest an anti-remodeling effect of training in patients with ischemic CHF. Eur J Cardiovasc Prev Rehabil 14: 85-91

Infarct size determines myocardial uptake of CD34+ cells in the peri-infarct zone: results from a study of (99m)Tc-extametazime-labeled cell visualization integrated with cardiac magnetic resonance infarct imaging.

Background— Effective progenitor cell recruitment to the ischemic injury zone is a prerequisite for any potential therapeutic effect. Cell uptake determinants in humans with recent myocardial infarction are not defined. We tested the hypothesis that myocardial uptake of autologous CD34+ cells delivered via an intracoronary route after recent myocardial infarction is related to left ventricular (LV) ejection fraction (LVEF) and infarct size. Methods and Results— Thirty-one subjects (age, 36–69 years; 28 men) with primary percutaneous coronary intervention–treated anterior ST-segment–elevation myocardial infarction and significant myocardial injury (median peak troponin I, 138 ng/mL [limits, 58–356 ng/mL]) and sustained LVEF depression at ⩽45% were recruited. On day 10 (days 7–12), 4.3×106 (0.7–9.9×106) 99mTc-extametazime–labeled autologous bone marrow CD34+ cells (activity, 77 MBq [45.9–86.7 MBq]) were administered transcoronarily (left anterior descending coronary artery). 99mTc-methoxyisobutyl isonitrile (99mTc-MIBI) single-photon emission computed tomography before cell delivery showed 7 (2–11) (of 17) segments with definitely abnormal/absent perfusion. Late gadolinium-enhanced infarct core mass was 21.7 g (4.4–45.9 g), and infarct border zone mass was 29.8 g (3.9–60.2 g) (full-width at half-maximum, signal intensity thresholding algorithm). One hour after administration, 5.2% (1.7%–9.9%) of labeled cell activity localized in the myocardium (whole-body planar &ggr; scan). Image fusion of labeled cell single-photon emission computed tomography with LV perfusion single-photon emission computed tomography or with cardiac magnetic resonance infarct imaging indicated cell uptake in the peri-infarct zone. Myocardial uptake of labeled cells activity correlated in particular with late gadolinium-enhanced infarct border zone mass (r=0.84, P<0.0001); it also correlated with peak TnI (r=0.76, P<0.001), severely-abnormal/absent perfusion segment number (r=0.45, P=0.008), and late gadolinium-enhanced infarct core (r=0.58, P=0.0003) but not with echocardiography LVEF (r=−0.07, P=0.68) or gated single-photon emission computed tomography LVEF (r=−0.28, P=0.16. The correlation with cardiac magnetic resonance imaging-LVEF was weak (r=−0.38; P=0.04). Conclusions— This largest human study with labeled bone marrow CD34+ cell transcoronary transplantation after recent ST-segment–elevation myocardial infarction found that myocardial cell uptake is determined by infarct size rather than LVEF and occurs preferentially in the peri-infarct zone.

Myocardial perfusion in hypertensive patients with normal coronary angiograms.

Background Pressure-induced left ventricular hypertrophy is one of the mechanisms responsible for an impaired coronary vasodilating capacity leading to myocardial ischemia and angina. The aim of the study was to investigate myocardial perfusion using cardiovascular magnetic resonance in patients with arterial hypertension and a history of chest pain and normal coronary angiography, and to estimate the influence of left ventricular hypertrophy on the parameters of myocardial perfusion. Methods The study included 102 patients (mean age 55.4 ± 7.7 years) with well controlled hypertension and 12 healthy volunteers. In 96 patients, myocardial first-pass perfusion cardiovascular magnetic resonance both at rest and during an infusion of adenosine 140 μg/kg/min was performed. Semiquantitative perfusion analysis was performed by using the upslope of myocardial signal enhancement to derive the myocardial perfusion index and the myocardial perfusion reserve index. The study group was divided according to the presence of left ventricular hypertrophy in the cardiovascular magnetic resonance examination: group with left ventricular hypertrophy (n = 40) and without left ventricular hypertrophy (n = 56). Results Independent of the presence of left ventricular hypertrophy, there were significant differences in baseline myocardial perfusion index between hypertensive patients and controls (0.13 ± 0.07 vs. 0.04 ± 0.01; P < 0.001), and in stress myocardial perfusion index (hypertensive patients 0.21 ± 0.10 vs. controls 0.09 ± 0.03; P < 0.001). In hypertensive patients, the myocardial perfusion reserve index was reduced in the mid and apical portions of the left ventricle (1.71 ± 1.1 vs. 2.52 ± 0.83; P < 0.02). There was no significant correlation of myocardial perfusion reserve index with left ventricular mass or hypertrophy. Conclusion In patients with mild or moderate hypertension and a history of chest pain with normal coronary angiography, there is regional myocardial perfusion reserve impairment that is independent of the presence of left ventricular hypertrophy and may be a reason for angina.

Osteoprotegerin, but not osteopontin, as a potential predictor of vascular calcification in normotensive subjects

We conducted a cross-sectional observation study that included 500 asymptomatic subjects to investigate the relationship between bone metabolism and coronary artery calcification (CAC) in hypertensive conditions. Osteoprotegerin (OPG) and osteopontin (OPN) levels and their associations with hypertension were analyzed to predict CAC in 316 subjects. Multislice computed tomography was used to quantify CAC. Multivariate analysis of variance was used to test the non-interactive effects of hypertension, CAC severity and biomarker levels, and the logistic regression model was applied to predict the risk of CAC. OPG and OPN concentrations were significantly higher in the hypertensive than the normotensive subjects, at 3.0 (2.3–4.0) pmol l−1 and 51 (21–136) ng ml−1 vs. 2.4 (2.0–3.0) pmol l−1 and 41 (13–63) ng ml−1, respectively. The OPG level, but not OPN level, increased with age (r=0.29; P=0.0001). Zero or minimal CAC (<10 Agatston units (AU)) was observed in 63% of the subjects, mild (11–100 AU) in 17%, moderate (101–400 AU) in 12% and severe (401–1000 AU)-to-extensive (>1000 AU) in 8%. In hypertensive subjects, only glomerular filtration rate (GFR) (β=−0.67) and gender (β=0.52) were significant predictors for CAC (R=0.68). In normotensive patients, GFR (β=−0.81), gender (β=0.48) and log-transformed OPG levels (β=0.15) were significant predictors for CAC. OPG levels were associated with an increased risk of CAC in normotensive subjects only (odds ratio: 3.37; 95% confidence interval (1.63–6.57); P=0.0002). OPG predicted a premature state of vascular calcification in asymptomatic normotensive individuals, and renal function significantly contributed to this process in both hypertensive and normotensive subjects.

Giant Pericardial Cyst Compressing the Right Ventricle

2008 by The Society of Thoracic Surgeons ublished by Elsevier Inc imensional transthoracic echocardiography revealed an bnormal mass compressing the right ventricular free wall. chocardiography imaging (Fig 1) from the subcostal view xhibited a large nonhomogenous mass (2.5 9.2 cm, red rrow) compressing the right ventricle (RV right ventricle; V left ventricle). The restrictive pattern of the transtriuspid flow with an increase of early maximal velocity early/atrial ratio, 2.43; deceleration time, 131 milliseconds) evealed the mechanism responsible for the right heart ecompensation. No significant valvular abnormalities ere identified. The chest roentgenogram revealed the right pleural ffusion and the effusion in the left cardiophrenic angle. ardiac dual-source computed tomography with threeimensional reconstruction volume-rendering technique emonstrated a giant paracardiac, well-delineated, capulated hypodense mass (10.5 7.5 cm) with calcificaions positioned anterior to the right ventricle (Fig 2). The eart and great vessels were otherwise normal. Convenional coronary angiography revealed the normal vessels. The patient was referred for a surgical removal of the yst. Intraoperatively, a giant pericardial cyst filled with artly hemolyzed blood and fibrin (600 g total), causing ardiac compression, was found and removed (Fig 3). The nterior part of pericardium was calcified, and the calcications were resected. The perioperative period was neventful and the patient was discharged home on the ig 3.

Risk Stratification in Dialysis Patients: Coronary Artery Calcification Score Combined with High Sensitive C-Reactive Protein and Framingham Score for Cardiovascular Risk Prediction in Asymptomatic Subjects

Introduction: Vascular calcification independently predicts cardiovascular disease, the major cause of death in Chronic Kidney Disease (CKD) patients. Coronary Artery Calcium Score (CACS) is a marker for atherosclerotic plaque burden, vascular calcification and has been shown to be a predictor of incidence of myocardial infarction and death from Cardiovascular (CV) disease. Objectives: The aim of the study was to evaluate factors influencing CV mortality in a group of Peritoneal Dialysis (PD) patients during a six year observation period. Patients and methods: The study included 53 patients with no symptoms of CV disease (25 women, 28 men; mean age of 52 ± 12 years) treated with PD for a median period of 24 months. Baseline Framingham Risk Score (FRS) was assessed and CACS was measured using Multi-Row Spiral Computed Tomography (MSCT). Laboratory measurements included high sensitive C-reactive protein (hsCRP), osteoprotegerin (OPG), fibroblast growth factor 23 (FGF23), osteopontin (OPN), osteocalcin (OC), intact parathyroid hormone (iPTH), total calcium (Ca) and phosphates (Pi). The data concerning mortality was collected over a 6 year period. Results: During the six year observation period, 24 (45%) patients died, including 19 due to CV causes. Median overall survival was 72 months (lower quartile, 17 months). CACS was a significant predictor of all-cause and CV mortality both in simple analysis (HR=1.03 per 100 Agatston units, p=0.02 and HR=1.05, p=0.003), as well as in a multiple model adjusted for age of patients, dialysis duration, weekly creatinine clearance, Ca x Pi, iPTH, OPG, hsCRP and FRS (HR=1.04, p=0.02 and HR=1.05, p=0.01). The value of 800 Agatston units significantly differentiated the group into those with higher and lower risk for CV death (p=0.04). Age and FGF23 concentration were independent predictors of CACS. Also, hsCRP and FRS significantly predicted all-cause and CV mortality in simple Cox regression (HR=1.04, p=0.002 and HR=1.04, p=0.003; HR=1.14, p=0.047 and HR=1.23, p=0.01) as well as in a multiple model (HR=1.05, p=0.002 and HR=1.05, p=0.01; HR=1.23, p=0.01 and HR=1.33, p=0.004). Adding CACS to FRS and hsCRP significantly improved the prediction of cardiovascular mortality (p=0.02). Conclusions: Coronary calcium imaging is a non-invasive method of CV risk stratification that can accurately identify high-risk asymptomatic dialysis patients at the start of dialysis. The assessment of CACS together with inflammatory markers and conventional CV risk factors (FRS) may contribute to early diagnosis, prevention and reduction of deaths from CV disease in dialysis patients. Among the markers of bone disease, FGF-23 (a regulator of phosphorus metabolism) may be an early predictor of vascular calcification among dialysis patients.