Evaluation of left ventricular circumferential contraction functions in obese patients.

BACKGROUND: We aim to evaluate left ventricular (LV) function abnormalities, especially circumferential contraction functions, in obese patients. METHOD: Cases without coronary artery disease (CAD) were divided into two groups according to their body mass indexes (BMI). RESULTS: Female predominance (P = 0.002), systolic blood pressure (BP) (P = 0.001), diastolic BP (P = 0.001), waist circumference (P < 0.001), left atrium (P < 0.001), LV end-diastolic diameter (P = 0.046), LV mass index (P = 0.001), and LV stroke volume (P = 0.016) were prominent in obese patients (BMI > or = 27). In obese patients, transmitral late velocity (P = 0.005) was prominent, and pulmonary vein antegrade diastolic velocity (PV-D) (P = 0.002) and mitral annular early diastolic pulsed-wave tissue Doppler imaging (pw-TDI) velocity (annular Ea) (P = 0.032) were lower. Transmitral late velocity was positively correlate with stroke volume (P = 0.029) and systolic BP (P < 0.001). Negatively correlation between PV-D and diastolic BP (P = 0.046) was found. And also, annular Ea velocity was negatively correlate with systolic BP (P = 0.017) and diastolic BP (P = 0.031). These findings may reflect LV longitudinal contraction abnormalities (LVLCA) and underlying mechanism that is responsible for LVLCA, may be volume and afterload alterations. However, LV circumferential contraction functions that evaluate by using pw-TDI, were not different among the groups. CONCLUSION: In obese patients without CAD, it was clearly said that while LVLCA were evident, LV circumferential contraction abnormalities were not. This differentiation may be explained by subepicardial myocardial fiber that is responsible for LV circumferential contractions is supplied by coronary arteries, subendocardial myocardial fiber that is responsible for LV longitudinal contractions, is supplied by systemic circulation via LV cavity penetration.

The association between left ventricular diastolic dysfunction and increased aortic stiffness can be explained by possible neurohumoral mechanisms.

OBJECTIVE: In our study, we tried to find an answer to the question "How could the association between left ventricular diastolic dysfunction (LVDDF) and increased aortic stiffness (IAS) be explained?" METHODS: Cases without coronary artery disease (CAD) were divided into three groups according to their left ventricular (LV) inflow patterns and their LV basal-lateral annulus pulsed-wave tissue Doppler imaging (pw-TDI). Group 1 (n = 38) represented the normal LV inflow pattern while Group 2 (n = 54) represented impaired LV relaxation and Group 3 (n = 18) represented pseudonormalization. Aortic diameters were measured by using M-mode at a level that is 3 cm above the aortic valve. Aortic strain (AS) and aortic distensibility (AD) were calculated by using aortic diameters and pulse pressure. RESULTS: In Group 3, AS was lower compared to Groups 1 and 2 (respectively P < 0.001, P = 0.040). AS was also lower in Group 2 compared to Group 1 (P = 0.012). AD was higher in Group 1 compared to Groups 2 and 3 (respectively P = 0.01, P < 0.001). Early diastolic velocity of aortic pw-TDI was higher in normal LV inflow compared to Groups 2 and 3 (respectively P = 0.022, P = 0.050). Unfortunately, none of echocardiographic parameters that evaluate LV and aortic functions together (stroke volume, pulse pressure/stroke volume, pulse pressure/stroke volume index) were different among the groups. CONCLUSION: The results of our study clearly showed the association between LVDDF and IAS in cases without CAD. Additionally, it was concluded that this togetherness could be explained not by hemodynamic factors but by possible neurohumeral mechanisms.

Intracoronary autologous bone marrow-derived mononuclear cell transplantation improves coronary collateral vessel formation and recruitment capacity in patients with ischemic cardiomyopathy: a combined hemodynamic and scintigraphic approach.

This study investigated the effects of intracoronary autologous bone marrow-derived mononuclear cell (BMC) transplantation on coronary microcirculation. Fifteen patients with ischemic cardiomyopathy were treated by intracoronary infusion of BMCs via the patent infarct-related artery. The thermodilution-derived coronary flow reserve, index of microvascular resistance, pressure-derived collateral flow index, and coronary wedge pressure were measured at baseline and at 6 months. Successive balloon inflations during BMC transplantation were performed to observe the recruitment in pressure-derived collateral flow index and coronary wedge pressure, and the percentage changes between baseline and 6 months were calculated. The mean (SD) coronary flow reserve increased from 1.3 (0.4) to 2.1 (0.5), and the mean (SD) index of microvascular resistance decreased from 44.9 (24.4) to 21.2 (14.1) (P = .001 for both). The mean (SD) improvement in pressure-derived collateral flow index (from 0.14 [0.05] to 0.22 [0.08]) was also statistically significant (P = .001). Similarly, the percentage improvements in pressure-derived collateral flow index and coronary wedge pressure were statistically significant (P = .01 for both). The percentage improvement in perfusion assessed by single-photon emission computed tomography strongly correlated with the percentage changes in pressure-derived collateral flow index (r = 0.88, P = .001) and coronary wedge pressure (r = 0.69, P = .01). These results demonstrate for the first time (to our knowledge) that intracoronary autologous BMC transplantation improves coronary collateral vessel formation and recruitment capacity in human subjects.

Metastatic Ewing's sarcoma involving the right ventricle.

Cardiac metastasis of Ewing's sarcoma is rare. A 22-year-old woman was admitted with complaints of palpitation and fatigue on exertion. She had a seven-year history of radical right tibial resection for Ewing's sarcoma and was also receiving chemotherapy for lung metastasis of Ewing's sarcoma. Both transthoracic and transesophageal echocardiography demonstrated a single, large (3x3.5 cm) inhomogeneous mass located in the free wall of the right ventricle. To differentiate the mass from a massive thrombus, contrast-enhanced magnetic resonance imaging was performed. The mass showed partial contrast enhancement, suggesting a malignant metastatic mass. Surgical resection was not considered due to accompanying lung metastasis and potentially poor outcome of the operation.

Echocardiographic diagnosis of a giant thrombus passing through a patent foramen ovale from right atrium to the left atrium.

Pulmonary embolus sourced by right atrial thrombus trapped in a patent foramen ovale is an unusual, rare condition. Thus in suspicion of massive pulmonary thromboembolus, echocardiographic examination carries great importance evaluate right ventricular functions and diagnose right sided intracardiac thrombus. We report a 76-year-old female with massive pulmonary embolism caused by a gigantic thrombus trapped in a patent foramen ovale. The echocardiography was the diagnostic procedure to display the source of the thromboembolism and urgent cardiac surgery was successful and life-saving treatment in this case.

Effects of different intensities of acute exercise on flow-mediated dilatation in patients with coronary heart disease.

It is known that regular exercise training improves endothelial dysfunction in coronary artery disease, but, little is known concerning different intensities of acute exercise on endothelial function. We evaluated anaerobic threshold and peak oxygen uptake level of acute exercise on flow-mediated dilatation in patients with stable coronary artery disease. Endothelium-independent vasoreactivity in patients showed a trend with increase at threshold level exercise; however, it was significantly decreased at peak level exercise. Moderate intensity exercise (nearly anaerobic threshold level) should be recommended a therapeutic and preventative strategy for starting of cardiac rehabilitation program in patients with coronary artery disease.

Aspirin-resistant platelet aggregation in a cohort of patients with coronary heart disease.

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.

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.)

Clinical relevance of aspirin resistance in patients with stable coronary artery disease: a prospective follow-up study (PROSPECTAR).

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.

Association of haematological indices with the degree of microvascular injury in patients with acute anterior wall myocardial infarction treated with primary percutaneous coronary intervention.

BACKGROUND: In acute myocardial infarction (AMI), increased neutrophil count has been associated with more severe coronary artery disease and larger infarct size. Increased mean platelet volume (MPV) is also associated with poor clinical outcome and impaired angiographic reperfusion in patients with AMI. However, the associations of neutrophil count and MPV with the indices of tissue level reperfusion were not fully elucidated. AIM: To elucidate the relationship between baseline neutrophil count and MPV on presentation and microvascular injury in patients with anterior AMI treated with primary percutaneous coronary intervention (pPCI). METHODS: 41 patients with anterior wall AMI treated successfully with pPCI were included. The leucocyte count, neutrophil count and MPV were obtained on admission, and the percentage of neutrophils was calculated. After PCI thrombolysis in myocardial infarction, grade 3 flow was established in all patients. The coronary flow velocity pattern (diastolic deceleration time (DDT)) was examined with transthoracic echocardiography and measured intracoronary pressures with fibreoptic pressure-temperature sensor-tipped guidewire in the left anterior descending artery within 48 h after pPCI. Thermodilution-derived coronary flow reserve (CFR) was calculated. Index of microvascular resistance (IMR) was defined as simultaneously measured distal coronary pressure divided by the inverse of the thermodilution-derived hyperaemic mean transit time. Subsequently, a short compliant balloon was placed in the stented segment and inflated to measure coronary wedge pressure (CWP). RESULTS: Higher neutrophil counts were strongly associated with higher IMR (r = 0.86, p<0.001), lower CFR (r = -0.60, p<0.001), shorter DDT (r = -0.73, p<0.001) and higher CWP (r = 0.73, p<0.001). Likewise, there were significant correlations among the percentage of neutrophils and CFR (r = -0.34, p = 0.02), IMR (r = 0.46, p = 0.002), DDT (r = -0.36, p = 0.01) and CWP (r = 0.49, p = 0.001). Relationships among leucocyte count and IMR (r = 0.38, p = 0.01), CFR (r = -0.33, p = 0.03), DDT (r = -0.36, p = 0.01) and CWP (r = 0.32, p = 0.026) were slightly significant. Higher neutrophil count remained independently associated with indices of microvascular perfusion in multivariable models controlling for age, smoking habits and time to treatment. Also, higher MPV on admission was strongly associated with higher IMR (r = 0.89, p<0.001), steeper DDT (r = -0.64, p<0.001), lower CFR (r = -0.43, p = 0.004) and higher CWP (r = 0.77, p<0.001). CONCLUSION: Absolute and relative neutrophilia and higher MPV on admission were independently associated with impaired microvascular perfusion in patients with anterior AMI treated with pPCI. It is possible that neutrophilia and high MPV are simple surrogate markers of worse microvascular injury in patients with AMI.

A potential evidence to explain the reason behind the devastating prognosis of coronary artery disease in uraemic patients: renal insufficiency is associated with poor coronary collateral vessel development.

The potential of individuals to develop coronary collateral circulation is often neglected but is of potential major importance in myocardial vulnerability. Likewise, the effect of chronic kidney disease (CKD) on collateral vessel development is not known. The purpose of this study was to evaluate the effect of CKD on collateral development in patients with advanced coronary artery disease. A total of 171 uraemic patients (serum creatinine > or = 1.5 mg/dl, creatinine clearance < 80 mL)/min) who underwent coronary angiography were evaluated in this study. A total of 134 patients met the criteria for the uraemic group and 134 consecutive non-uraemic patients who constituted the control group. The collateral score (CS) was graded according to the Rentrop classification and the collateral score was calculated by summing the Rentrop numbers of every patient. Collateral vessels have also been categorized according to their anatomic locations and collateral connection grades (CC). CC2 collaterals were observed less frequently in the uraemic patients than in the control subjects (11% versus 26%, p=0.03) and CC0 more frequently (31% versus 22%, p<0.05). Epicardial pathway was detected more frequently in the control subjects than in the uraemic patients (31% versus 12%, p=0.03) and septal pathway less frequently (37% versus 54%). There was a significant negative correlation between CS and creatinine (r=-0.68, p<0.01). The mean CS in the uraemic group was significantly lower than the non-uraemic group (1.29+/-0.88 versus 2.18+/-1.3, p<0.001). These results altogether showed that besides the quantity, quality (functional, haemodynamic and anatomic features) of the uraemic collaterals and a network that they constitute is also impaired and different from the collaterals of the patient with normal renal function.

The use of human heart-type fatty acid-binding protein as an early diagnostic biochemical marker of myocardial necrosis in patients with acute coronary syndrome, and its comparison with troponin-T and creatine kinase-myocardial band.

Heart-type fatty acid-binding protein (H-FABP), a new biochemical marker of sarcolemmal injury due to acute myocardial ischemia, can be used as a tool in early diagnosis and management of patients at high risk. The aim of this study was to determine the early diagnostic value of H-FABP in acute coronary syndrome (within 6-24 h of chest pain) and to compare it with troponin-T (TnT) and creatine kinase-myocardial band (CK-MB) for accuracy. The study consisted of 40 consecutive patients with chest pain admitted to the coronary care unit with the diagnosis of suspected acute coronary syndrome. The patient population consisted of two groups according to the time of admission; the first group (26 patients) included patients admitted within 6 h of chest pain, and the second group (14 patients) included patients admitted within 6-24 h of chest pain. The blood samples for H-FABP, TnT, and CK-MB were obtained at admittance, at the 6th, and at the 24th hours for the first group, and at admittance and at the 24th hours for the second. Statistical analysis was performed among the 26 patients for the first 6 h values, and among all 40 patients for the values obtained within 6-24 h and at the 24th hour. The patients were then divided into groups according to the changes in the electrocardiogram (ECG) and cardiac enzymes as unstable angina pectoris, non-ST elevation myocardial infarction (MI), and ST-elevation MI. Coronary angiography was performed in 38 (95%) patients. Sensitivity of TnT, CK-MB, and H-FABP in the first group (within 6 h of chest pain) were 38%, 76%, and 95% respectively. The sensitivity of H-FABP was significantly higher than TnT (P=0.014). Sensitivity of TnT, CK-MB, and H-FABP tests in the second time period (within 6-24 h of chest pain) were 100%, 90%, and 91% respectively. In this time period, the sensitivity of TnT was higher than H-FABP, but it was statistically insignificant. At the 24th hour, sensitivity of TnT was 100%, CK-MB 90%, and H-FABP 27.3%, and TnT and CK-MB were more sensitive than H-FABP for the whole group (P=0.002). In the first group (within 6 h of chest pain) H-FABP positivity was slightly but insignificantly higher in patients with two- and three-vessel disease compared with those with one-vessel disease (60.7% and 33.3%, P=0.19) and in the same group, patients who underwent primary coronary intervention had a significantly higher H-FABP positivity than others (80%, 32%, P=0.02). Within 6-24 h of chest pain, H-FABP positivity was 80% in patients with one-vessel disease and 71.4% in patients with two- and three-vessel disease (P=0.69). Within 6-24 h, positivity of H-FABP reached a peak value of 100% in patients who underwent primary coronary intervention, while H-FABP was positive in 60% of the others (P<0.001). We conclude that within the 6 h of acute coronary syndrome, H-FABP seems to be a more sensitive biochemical marker than TnT in the early detection of ischemic myocardial necrosis. But after the first 6 h of the onset of chest pain the sensitivity of H-FABP decreases, and this marker should not be used alone in patients admitted 24 h after the onset of chest pain.

The role of aspirin resistance on outcome in patients with acute coronary syndrome and the effect of clopidogrel therapy in the prevention of major cardiovascular events.

BACKGROUND: Aspirin resistance may increase up to more then threefold the risk of major cardiovascular events (MACE) in patients with stable coronary artery disease. AIM: The aim of our study was to determine; the prevalence of aspirin resistance in patients with acute coronary syndromes, the role of aspirin resistance on outcome in the follow-up and the effect of clopidogrel therapy in the prevention of MACE in aspirin resistant subjects. MATERIAL AND METHODS: We detected the prevelance of aspirin resistance in 105 patients with acute coronary syndrome. Platelet functions were analyzed in Platelet Function Analyzer (PFA)-100 (Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or ADP (Col/ADP) cartridges. Primary end points of the study were myocardial infarction, unstable angina, cardiac death. RESULTS: 19% (n = 20) of patients were aspirin resistant by PFA-100. In the follow-up, MACE occured in 9 patients (45%) with aspirin resistance and in 10 patients (11.7%) with aspirin sensitive platelet aggregation (p = 0.001). Multivariate analysis showed that aspirin resistance was an independant predictor of MACE. The prevalence of MACE in patients who were on clopidogrel treatment for 12 months were lower compared to those who were on a clopidogrel treatment for the first six months (p = 0.040). CONCLUSIONS: We determined that the MACE risk in patients with acute coronary syndromes having detected aspirin resistance, was higher at statistically significant levels compared to patients having aspirin sensitive platelet aggregation. Our results showed that aspirin resistance, was an independant predictor of MACE in patients with acute coronary syndrome.

Endothelial function in patients with obstructive sleep apnea syndrome but without hypertension.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) influences endothelial function and causes hypertension. OBJECTIVES: Our aim was to evaluate the role of endothelial dysfunction in the pathogenesis of hypertension in OSAS. METHODS: Twenty-three patients with OSAS but without hypertension and 15 healthy normotensive subjects were investigated. The presence or absence of OSAS was evaluated with a sleep study. Endothelial function was investigated with brachial artery ultrasound examination. RESULTS: Baseline characteristics were equivalent between the two groups. Minimal oxygen saturation and apnea-hypopnea indexes in the OSAS and control groups were 62.9 +/- 16.5 versus 94.9 +/- 1.1% (p < 0.0001) and 53.1 +/- 20.3 versus 3.8 +/- 0.9 (p < 0.0001), respectively. There was not statistically significant difference between basal brachial artery diameters measured in the morning and in the evening in all groups. Flow-mediated dilation (FMD) values measured in the morning were lower than those measured in the evening in both OSAS patients and the control group: FMD of OSAS patients was 6.04 +/- 3.18% in the morning and 10.38 +/- 4.23% in the evening hours (p = 0.001), and FMD of control subjects was 10.9 +/- 2.6% in the morning and 13.9 +/- 2.32 in the evening hours (p = 0.002). Differences in FMD values measured both in the morning and evening hours in OSAS patients were lower compared with those in control subjects (p < 0.0001 in the morning hours and p = 0.003 in the evening hours). CONCLUSIONS: We detected a prominent diurnal deterioration in endothelial function in normotensive OSAS patients compared with healthy subjects. This deterioration may occur due to ongoing hypoxemia during the night and it may be a possible cause of hypertension and atherosclerotic cardiovascular diseases in patients with OSAS.

Multiple coronary thrombosis and stent implantation to the subtotally occluded right renal artery in a patient with essential thrombocytosis: a case report with review.

Essential thrombocytosis is a myeloproliferative disorder of unknown etiology manifested clinically by the overproduction of platelets in the absence of a definable cause. Platelet dysfunction in essential thrombocytosis results in both hemorrhage and thrombosis. It is one of the rare causes of ischemic cardiovascular events. Fewer than 20 cases of essential thrombocytosis with involvement of coronary arteries leading to acute coronary syndromes or myocardial infarction have been reported. We report a case of multiple coronary thrombosis involving the left anterior descending artery and circumflex artery and stent implantation to the subtotally stenotic right renal artery in a women with unstable angina pectoris, essential thrombocytosis and previous history of renal artery trombosis.

Cardiac fatigue and oxygen kinetics after prolonged exercise.

BACKGROUND: Although the underlying mechanisms responsible for cardiac dysfunction after prolonged exercise remains to be elucidated, it has reported cardiac deterioration following exhaustive exercise in the absence of underlying cardiovascular diseases, which has been attributed to cardiac fatigue. The study was designed to investigate the effects of after fatiguing exercise on oxygen kinetics. METHODS: Six athletes have taken examination, firstly by echocardiography, secondly by cardiopulmonary exercise testing and then by near-infrared spectroscopy (NIRS), before 2 days (pre-race) and after 1 day (post-race) marathon competition. RESULTS: We found decrease in left ventricular systolic and diastolic functions, and peak oxygen consumption while increasing half time of muscular oxygen delivery after race period. CONCLUSION: Cardiopulmonary exercise testing in conjunction with oxygen kinetics of skeletal muscle measured by NIRS may be a tool for detecting cardiac fatigue.

Pressure-derived collateral flow index: a strong predictor of late left ventricular remodeling after thrombolysis for acute myocardial infarction.

OBJECTIVE: Despite proved efficacy of pressure-derived collateral flow index in determining microvascular dysfunction in patients with acute myocardial infarction, its role in prediction of left ventricular remodeling at long term has yet to be demonstrated. In this study, we investigated the relationship between quantitatively assessed microvascular dysfunction by using intracoronary pressure wire and late left ventricular remodeling. PATIENTS AND METHODS: The study population consisted of 28 patients with first acute myocardial infarction. They were treated with fibrinolytic therapy. The inclusion criteria were thrombolysis in myocardial infarction grade II-III flow in infarct-related artery and all destined for stent implantation. Cardiac catheterization and stent implantation were performed in mean of 3.3 days after acute myocardial infarction. During the stent implantation procedure, the pressure-derived collateral flow index was measured by using intracoronary pressure wire. Control angiograms were performed at 6+/-2 months. Echocardiographic left ventricular volume indexes were measured at discharge, at 6 months and at 1 year. Changes in left ventricular volumes from baseline to 1 year were followed. RESULTS: Left ventricular end-diastolic volume index at 1 year correlated significantly with the pressure-derived collateral flow index (r=0.69, P<0.01). A significant correlation was also observed between the change in left ventricular end-diastolic volume index from baseline to 1 year and the pressure-derived collateral flow index (r=0.65, P<0.01). The most important predictor of 1-year left ventricular remodeling was the pressure-derived collateral flow index (P<0.0001), and collateral circulation (P=0.03). CONCLUSION: The pressure-derived collateral flow index is a powerful independent predictor of 1-year left ventricular dilatation. Given its simplicity of measurement, and correlation with microvascular obstruction and left ventricular outcome at long term, the pressure-derived collateral flow index may provide useful and valuable estimates of clinical outcomes after acute myocardial infarction.