Peak Creatine Phosphokinase Research Articles

Decreased Serum Ghrelin Levels in Patients with Acute Myocardial Infarction

Ghrelin is a novel growth hormone-releasing peptide isolated from the stomach and possesses various cardioprotective effects, including energy balance improvement and regulation of autonomic nervous system activity. We investigated the changes in serum ghrelin levels and its association with cardiac function and myocardial infarct size in patients with acute myocardial infarction (AMI). Forty-seven consecutive patients were divided into the following 4 groups: 16 patients with AMI, 12 patients with unstable angina pectoris (UAP), 13 patients with stable angina pectoris (SAP), and 6 control patients. Serum levels were measured with the ELISA kit. Compared to the control (72 ± 26 fmol/mL), SAP (69 ± 47 fmol/mL), and UAP (72 ± 31 fmol/mL) groups, serum ghrelin levels on admission were significantly lower in the AMI group (27 ± 12 fmol/mL, P < 0.01). After admission, the serum ghrelin level gradually increased (30 ± 15 fmol/mL on day 2 and 39 ± 18 fmol/mL on day 7) and became significantly higher on day 14 (49 ± 28 fmol/mL, P < 0.01), compared to the level on admission. In patients with AMI, the ratio of day 14 to admission serum ghrelin levels, an index of AMI-related acute changes in ghrelin, correlated positively with peak creatine phosphokinase levels (R = 0.72, P < 0.01) and the double products (R = 0.60, P < 0.01) and inversely with left ventricular ejection fraction (R = -0.53, P < 0.05). In conclusion, serum ghrelin levels are significantly decreased in association with myocardial infarct size and cardiac function.

Prognostic impact of pulse pressure at admission on in-hospital outcome after primary percutaneous coronary intervention for acute myocardial infarction

Data regarding relationship between pulse pressure (PP) at admission and in-hospital outcome in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are still lacking. A total of 1413 primary PCI-treated AMI patients were classified into quintiles based on admission PP (<40, n = 280; 40-48, n = 276; 49-57, n = 288; 58-70, n = 288; and ≥71 mmHg, n = 281). The patients with PP < 40 mmHg tended to have higher prevalence of male, smoking, and Killip class ≥3 at admission; right coronary artery, left main trunk (LMT), or multivessels as culprit lesions; larger number of diseased vessels; lower Thrombolysis in Myocardial Infarction (TIMI) grade in the infarct-related artery before/after primary PCI; and higher value of peak creatine phosphokinase concentration. Patients with PP < 40 mmHg had highest mortality, while patients with PP 49-57 mmHg had the lowest: 11.8 % (<40), 7.2 % (40-48), 2.8 % (49-57), 5.9 % (58-70), and 6.0 % (≥71 mmHg). On multivariate analysis, Killip class ≥3 at admission, LMT or multivessels as culprit lesions, chronic kidney disease, and age were the independent positive predictors of the in-hospital mortality, whereas admission PP 49-57 mmHg, hypercholesterolemia, and TIMI 3 flow before/after PCI were the negative ones, but admission PP < 40 mmHg was not. These results suggest that admission PP 49-57 mmHg might be correlated with better in-hospital prognosis in Japanese AMI patients undergoing primary PCI.

Prognostic impact of systolic blood pressure at admission on in-hospital outcome after primary percutaneous coronary intervention for acute myocardial infarction

Data regarding the relationship between systolic blood pressure (SBP) at admission and in-hospital outcome in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) are still lacking in Japan. A total of 1475 primary PCI-treated AMI patients were classified into quintiles based on admission SBP (<105 mmHg, n=300; 105-125 mmHg, n=294; 126-140 mmHg, n=306; 141-158 mmHg, n=286; and ≥159 mmHg n=289). The patients with SBP<105 mmHg tended to have higher age, previous myocardial infarction, chronic kidney disease (CKD), Killip class≥3 at admission, right coronary artery, left main trunk (LMT), or multivessels as culprit lesions, larger number of diseased vessels, lower Thrombolysis In Myocardial Infarction (TIMI) grade in the infarct-related artery before primary PCI, and higher value of peak creatine phosphokinase concentration. Patients with SBP<105 mmHg had a significantly higher mortality, while mortality was not significantly different among the other quintiles: 24.3% (<105 mmHg), 4.8% (105-125 mmHg), 4.9% (126-140 mmHg), 2.8% (141-158 mmHg), and 5.2% (≥159 mmHg) (p<0.001). On multivariate analysis, Killip class≥3 at admission, LMT or multivessels as culprit lesions, admission SBP<105 mmHg, CKD, and age were the independent positive predictors of in-hospital mortality, whereas admission SBP 141-158 mmHg and TIMI 3 flow after PCI were the negative ones, but admission SBP 105-125 mmHg, admission SBP 126-140 mmHg, and admission SBP≥159 mmHg were not. These results suggest that admission SBP 141-158 mmHg might be correlated with better in-hospital prognosis, whereas admission SBP<105 mmHg was associated with in-hospital death in Japanese AMI patients undergoing primary PCI.

Traumatic Aortic Injuries Associated with Major Visceral Vascular Injuries in Major Blunt Trauma Patients

The objectives of this study were to report the clinical and radiological characteristics and outcomes of a series of acute traumatic aortic injuries (ATAIs) with associated injury to major aortic abdominal visceral branches (MAAVBs). From January 2000 to August 2011, 10 consecutive major blunt trauma patients with associated ATAI and injury to MAAVBs (group A) and 42 major blunt trauma patients presenting only an ATAI without MAAVB injuries (group B) were admitted to our institution. Overall in-hospital mortality was 32.7%. In-hospital mortality in group A was 40% and in group B it was 31% (p = 0.86). Observed in-hospital mortality was slightly lower than the expected in-hospital mortality in both groups. Mean peak creatine phosphokinase was significantly higher in group A than in group B patients (23,008 ± 33,400 vs. 3,970 ± 3,495 IU/L; p < 0.001). Acute renal injury occurred in 50% of group A and in 26.2% of group B patients. Hemodiafiltration was required in 30% of group A and in 9.5% of group B patients. Median follow-up time was 64 months (range = 1-130 months). Group A survival was 60% at 1, 5 and 10 years. Group B survival was 69% at 1 year and 63.3% at 5 and 10 years (p = 0.15). Aortic injuries associated with MAAVB injuries in major trauma patients seem to present in a different clinical scenario. These patients present increased risk of rhabdomyolysis, visceral ischemia, and acute renal failure, as well as higher in-hospital mortality. A multidisciplinary approach combining endovascular and open surgical techniques for a staged treatment of these life-threatening aortic and MAAVB injuries is mandatory in this critical subset of trauma patients.

Aortic injuries in crush trauma patients: Different mechanism, different management

BackgroundThe objective of this study is to report the clinical and radiological characteristics and early and long-term survival of a series of acute traumatic aortic injuries (ATAI) in crush trauma patients, and to compare such data with our last 30 years experience managing ATAI in deceleration non-crush trauma patients. MethodsFrom January 1980 to December 2010, 5 consecutive ATAI in crush trauma and 69 in non-crush trauma patients were admitted at our institution. ISS, RTS and TRISS scores were similar in both groups. ResultsOverall in-hospital mortality was 24.3%. There was no in-hospital mortality in crush patients and 26.1% in non-crush patients (p=0.32).All aortic-related complications occurred in non-crush patients. Median follow-up was 129 months (range 3–350 months). Non-crush group survival was 76.8% at 1 year, 73.6% at 5 years, and 71.2%% at 10 years. There was no mortality during follow-up in the crush group. Mean (SD) peak creatine phosphokinase was significantly higher in crush group than in non-crush group: 7598 (3690)IU/L vs. 3645 (2506)IU/L; p=0.041. Incidence of acute renal injury was higher in crush trauma patients (100% vs. 36.2%; p=0.018). Low-severity injuries were more common in crush trauma patients (100% in crush patients vs. 43.5% in non-crush patients, p=0.04). ConclusionsAortic injuries in crush thoracic trauma patients seem to present in a different clinical scenario from aortic injuries in high-speed thoracic trauma thus requiring distinct considerations. When planning the initial management of aortic injuries in crush trauma, the increased risk of rhabdomiolysis and subsequent acute renal failure, as well as a tendency to develop lower-risk aortic wall injuries, must be considered.

Matrix Metalloproteinase 9 Polymorphism and Outcome after Myocardial Infarction

Matrix metalloproteinase 9 (MMP9) is functionally implicated in the process of infarct healing. Several genetic variation of the MMP9 gene have been described, among which the MMP9 Arg668Gln polymorphism. In the present study, we assessed whether this polymorphism influences outcome after acute myocardial infarction (MI). One thousand forty-nine patients undergoing coronary angiography were genotyped for the MMP9 Arg668Gln polymorphism by TaqMan allelic discrimination assay. This population included 154 controls, 161 patients with non ST-elevation MI (NSTEMI), 504 patients with ST-elevation MI (STEMI), and 230 patients with angina. Frequency of the MMP9 Arg668Gln polymorphism in the global population was 25.1%, and was comparable between all groups. STEMI patients had higher creatine phosphokinase (CPK), troponin T (TnT) and MMP9 plasma levels and had lower ejection fraction (EF) than NSTEMI patients. However, the polymorphism was not associated with infarct severity as determined by peak CPK and TnT levels, nor with LV remodeling and outcome as assessed by 1-month EF and NYHA class, as well as 2- year mortality. In silico molecular modeling simulations predicted that the MMP9 polymorphism may decrease MMP9 activity, but this could not be verified by plasma determinations. This study investigated for the first time the association between the MMP9 Arg668Gln polymorphism and clinical outcome after acute MI. Our results indicate that the polymorphism does not seem to be associated with clinical outcome and in particular with the development of left ventricular dysfunction and heart failure.

Systolic blood pressure at admission, clinical manifestations, and in-hospital outcomes in patients with acute myocardial infarction

Several clinical studies have demonstrated an inverse relationship between systolic blood pressure (SBP) at admission and in-hospital mortality in patients hospitalized for acute myocardial infarction (AMI). However, data on the relation between admission SBP and in-hospital prognosis in AMI patients are still lacking in Japan. A total of 1211 AMI patients were classified into quintiles based on SBP at hospital admission (<106 mmHg, n = 241; 106-125 mmHg, n = 239; 126-140 mmHg, n = 244; 141-159 mmHg, n = 238; and ≥ 160 mmHg, n = 249). The patients with SBP < 106 mmHg tended to have higher age, Killip class ≥ 3 at admission, right coronary artery, left main trunk, or multivessels as culprit lesions, larger number of diseased vessels, lower Thrombolysis In Myocardial Infarction grade in the infarct-related artery before primary percutaneous coronary intervention (PCI), and higher value of peak creatine phosphokinase concentration. Patients with SBP <106 mmHg had a significantly higher mortality, while mortality was not significantly different among the other quintiles: 25.7% (<106 mmHg), 5.4% (106-125 mmHg), 5.7% (126-140 mmHg), 2.5% (141-159 mmHg), and 5.6% (≥ 160 mmHg) (p<0.001). On multivariate analysis, Killip class ≥ 3 at admission, admission SBP <106 mmHg, and age were the independent positive predictors of in-hospital mortality, whereas admission SBP 141-159 mmHg and primary PCI were the negative ones, but admission SBP 106-125 mmHg, admission SBP 126-140 mmHg, and admission SBP ≥ 160 mmHg were not. These results suggest that admission SBP 141-159 mmHg might be correlated with better in-hospital prognosis, whereas admission SBP <106 mmHg was associated with in-hospital death in Japanese patients hospitalized for AMI.

Rhabdomyolysis associated with kava ingestion

We report a case of rhabdomyolysis temporally related to the ingestion of a large amount of kava. Kava is a naturally occurring plant used in the United States and elsewhere in the world for its sedative properties. A previous case report also related rhabdomyolysis to the ingestion of kava. It is not clear whether this is an action of the kava itself, perhaps, due to its action on voltage ion channels or, perhaps, due to an adulterant in the product. Our patient developed peak creatine phosphokinase levels in excess of 30 000 U/L but had no significant renal damage.

Long-term Follow-up of Patients Undergoing Postconditioning During ST-Elevation Myocardial Infarction

Reperfusion injury may offset the optimal salvage of myocardium achieved during primary coronary angioplasty. Thus, coronary reperfusion must be combined with cardioprotective adjunctive therapies in order to optimize myocardial salvage and minimize infarct size. Forty-three patients with their first ST-elevation myocardial infarction were randomized to myocardial postconditioning or standard of care at the time of primary coronary angioplasty. Postconditioning was performed immediately upon crossing the lesion with the guide wire and consisted of four cycles of 30 s occlusion followed by 30 s of reperfusion. End-points included infarct size, myocardial perfusion grade (MPG), left-ventricular ejection fraction (LVEF), and long-term clinical events (death and heart failure). Despite similar ischemic times (≅4.5 h) (p = 0.9) a reduction in infarct size was observed among patients treated with the postconditioning protocol. Peak creatine phosphokinase (CPK), as well as its myocardial band (MB) fraction, was significantly lower in the postconditioning group when compared with the control group (CPK--control, 2,444 ± 1,928 IU/L vs. PC, 2,182 ± 1,717 IU/L; CPK-MB--control, 242 ± 40 IU/L vs. PC, 195 ± 33 IU/L; p = 0.64 and p < 0.01, respectively). EF in the postconditioning group was improved when compared with the control group (control, 43% ± 15 vs. PC, 52% ± 9; p = 0.05). After a mean follow-up of 3.4 years, a 6-point absolute difference in LVEF was still evident in the postconditioning group (p = 0.18). MPG was better among patients treated with the postconditioning protocol compared with control (2.5 ± 0.5 vs. 2.1 ± 0.6; p = 0.02). Due to the small sample size no significant differences in clinical events were detected (p value for death = 0.9; p value for heart failure = 0.2). A simple postconditioning protocol applied at the onset of mechanical reperfusion, resulted in reduction of infarct size, better epicardial and myocardial flow, and improvement in left ventricular function. The beneficial effects of postconditioning on cardiac function persist beyond 3 years.

The First Clinical Pilot Study of Intravenous Adrenomedullin Administration in Patients With Acute Myocardial Infarction

Adrenomedullin (AM) is a 52-amino-acid vasodilator peptide that was originally isolated from human pheochromocytoma. In the previous experimental study with rat ischemia/reperfusion model, AM reduced infarct size and inhibited myocyte apoptosis. AM also suppressed the production of oxygen-free radicals. The present study was designed to evaluate the feasibility of intravenous administration of AM in patients with acute myocardial infarction. We studied 10 patients with first acute myocardial infarction [male to female ratio: 9 to 1, age: 65 ± 9 (mean ± SD) years, peak creatine phosphokinase level: 4215 ± 1933 (SD) U/L], who were hospitalized within 12 hours of symptom onset. Proceeding reperfusion therapy, AM infusion was initiated and continued at concentration of 0.0125-0.025 μg·kg·min for 12 hours. Follow-up coronary angiography and left ventriculography were performed at 3 months. Cardiac magnetic resonance was examined at 1 month and 3 months after AM therapy. During infusion of AM, hemodynamics kept stable except 2 patients. Wall motion index in the infarct area at 3 months was significantly improved compared with that at baseline, and infarct size evaluated by cardiac magnetic resonance was significantly decreased at 3 months. In conclusion, intravenous administration of AM, which possesses a variety of potential cardiovascular protective actions, can be adjunctive to percutaneous coronary intervention.

Value of a new multiparametric score for prediction of microvascular obstruction lesions in ST-segment elevation myocardial infarction revascularized by percutaneous coronary intervention

Despite improvement in revascularization strategies, microvascular obstruction (MO) lesions remain associated with poor outcome after ST-segment elevation myocardial infarction (STEMI). To establish a bedside-available score for predicting MO lesions in STEMI, with cardiac magnetic resonance imaging (CMR) as the reference standard, and to test its prognostic value for clinical outcome. Patients with STEMI of<12 hours' evolution treated by percutaneous coronary intervention (PCI) were included. CMR was performed 4-8 days later, to measure myocardial infarction (MI) extent, left ventricular ejection fraction (LVEF) and volumes, and to identify MO lesions. An MO score was built from multivariable logistic regression results and included clinical, angiographic and electrocardiographic criteria. Adverse cardiovascular events were recorded prospectively after STEMI. We analysed data from 112 patients. MO lesions were found in 63 (56%) patients and were associated with larger MI as assessed by higher peak creatine phosphokinase (3755 ± 351 vs 1467 ± 220 IU, p<0.001), lower LVEF (46.7 ± 1.5 vs 53.4 ± 1.6%, p<0.01) and larger MI extent (18.7 ± 1.2 vs 9.0 ± 1.3% LV, p<0.001) on CMR. MO score>4 accurately identified microcirculatory injuries (sensitivity 84%; specificity 82%) and independently predicted the presence of MO lesions on CMR. MO score>4 predicted adverse cardiovascular events during the first year after STEMI (relative risk 2.60 [1.10-6.60], p=0.03). MO lesions are frequent in PCI-treated STEMI and are associated with larger MIs. MO score accurately predicted MO lesions and identified patients with poor outcome post-STEMI.

The risk of non-sustained ventricular tachycardia after percutaneous alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy

Percutaneous alcohol septal ablation (ASA) becomes an alternative option of treatment for symptomatic patients with hypertrophic obstructive cardiomyopathy (HOCM). The procedure relieves left ventricular outflow tract obstruction, but produces a myocardial scar in patients who already have a substrate for life-threatening ventricular arrhythmia. To examine the effect of ASA on the occurrence of non-sustained ventricular tachycardia (nsVT) on 24 h ambulatory Holter monitoring in HOCM patients. Sixty-one consecutive patients (34 males, mean age 48 years), who underwent ASA between 1997 and 2003 were analyzed. Holter recordings were performed in each patient before and after ablation. Follow-up ranged from 60 to 125 months (median 116 months). The mean number of Holter recordings per patient was 2.7 (range 1-11) before and 8.3 (range 2-23) after ASA (p < 0.001). Non-sustained ventricular tachycardia occurred in 14 patients before and 27 patients after ASA (23 vs. 44%, p = 0.01). The percentage of Holter recordings with nsVT before and after ablation was similar (14.5 vs. 15.7%, p = 0.56, respectively). No difference was observed between the number of nsVT per Holter recording before and after ablation (0.21 vs. 0.24%, p = 0.65, respectively). The percentage of patients with nsVT after ASA was comparable to the proportion of patients with nsVT in a control group consisting of 705 patients with hypertrophic cardiomyopathy under follow-up at our institution (44.3 vs. 43.2%, p = 0.91). There was no significant difference in percentage of Holter recordings with nsVT with respect to sex, amount of alcohol used during ASA, peak creatine phosphokinase level, and gradient reduction at rest. Alcohol septal ablation affected neither the percentage of Holter recordings with nsVT nor the number of nsVT episodes per Holter recording among HOCM patients.

Prognostic Value of R-Wave Voltage in Patients With Anterior Wall ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

The prognostic value of integrated R-wave voltages of precordial leads (V(1)-V(6)) in patients with acute anterior wall ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) was investigated. Between July 2006 and October 2009, 292 patients with anterior wall STEMI with presentation < 12 hours underwent primary PCI. Thirty-four patients with electrocardiographic presentation of either complete right bundle branch block (BBB) or complete left BBB were categorized into group A, while the remaining 258 patients without BBB served as group B that was further subdivided into those with lower R-wave voltage (summation of V(1)-V(6) ≤ 1.7 mV) (group 1) and higher voltage (> 1.7 mV) (group 2) according to the ROC curve (sensitivity = 66.3%, specificity = 66%, P < 0.0001).While the procedural success rate was similar between groups A and B and groups 1 and 2, 30-day mortality was higher in group A than B (P ≤ 0.0001). Additionally, left ventricular ejection fraction (LVEF) was lower, whereas peak level of creatine phosphokinase (CPK), incidence of advanced congestive heart failure, and 30-day mortality were higher in group 1 than 2 (P < 0.01). Multivariate analysis revealed that lower R-wave voltage, multivessel disease, leukocyte count, peak CPK, and creatinine level were predictive of 30-day unfavorable clinical outcomes (all P < 0.01). R-wave voltage in precordial leads was a significant independent predictor of 30-day prognostic outcome in patients with anterior wall STEMI undergoing primary PCI.

Higher Serum Uric Acid on Admission Is Associated with Higher Short-term Mortality and Poorer Long-term Survival After Myocardial Infarction: Retrospective Prognostic Study

To assess serum uric acid (SUA) levels determined on admission as a potential predictor of short-term mortality and long-term survival in acute myocardial infarction (AMI) patients. Data for this retrospective prognostic study were drawn from the patient database of the Varazdin County General Hospital in Varazdin, Croatia. We included consecutive patients with verified AMI admitted within 48 hours since the symptom onset during the period between 1 January 1996 and 31 December 2001. Long-term survival/mortality data were collected through direct contacts with patients and search of the community death registries. Relative risks (RR) and hazard ratios (HR) by 10 micromol/L increase in SUA were determined using modified Poisson regression with robust error variance and proportional hazard regression, respectively. A total of 621 patients (age 27-90 years, 64.7% men, 77.5% AMI with ST elevation, SUA 63-993 micromol/L) were included. Higher SUA on admission was independently associated with higher in-hospital mortality (RR, 1.016; 95% confidence interval [CI], 1.001-1.031, P=0.043) and higher thirty-day mortality (RR, 1.016; 95% CI, 1.003-1.029, P=0.018). Considered covariates were demographics, pre-index event cardiovascular morbidity and treatment, on-admission serum creatinine, total cholesterol and triglycerides, AMI characteristics, and peak creatine phosphokinase. Higher SUA on admission was also independently associated with poorer long-term survival (ie, higher all-cause mortality) (HR, 1.105; 95% CI, 1.020-1.195, P=0.010). Considered covariates were demographics, laboratory variables on admission, AMI characteristics, peak creatine phosphokinase, acute complications, and treatment at discharge. Higher serum uric acid determined on admission is associated with higher in-hospital mortality and thirty-day mortality and poorer long-term survival after AMI.

Malignant Ventricular Arrhythmias in Patients With Acute Right Ventricular Infarction Undergoing Mechanical Reperfusion

Patients with acute right ventricular (RV) infarctions are prone to ventricular arrhythmias, but little is known regarding the temporal patterns of these arrhythmias, their impact on outcomes, or their relation to the severity of RV impairment. The aim of this study was to examine the impact of malignant ventricular arrhythmias (MVAs) complicating acute RV infarction. A further aim was to determine whether the degree of RV impairment was a predisposing factor to MVAs. The charts of 48 patients with acute RV infarctions were reviewed for documented MVAs. Temporal presentation, relating to reperfusion, and in-hospital outcomes were tabulated. Echocardiograms were reviewed to quantify RV impairment. MVAs occurred in 38% of patients, with multiple episodes (electrical storm) in 8.3%. MVAs developed before reperfusion (72% of patients), abruptly with reperfusion (11%), or after reperfusion (22%). Patients with MVAs had larger infarcts (peak creatine phosphokinase 3,027 vs 1,848 U/L, p = 0.03) and trended toward worse RV function (fractional shortening 27% vs 34%, p = 0.08). In-hospital mortality (patients with MVAs 17% vs 6.7%, p = 0.35), intensive care days (patients with MVAs 7.1 +/- 10 vs 3.9 +/- 2.5, p = 0.39), and hospital days (patients with MVAs 10.3 +/- 10 vs 8.0 +/- 5.1, p = 0.57) were similar between groups. Patients with electrical storm had longer intensive care stays (18.0 +/- 18.5 vs 4.0 +/- 2.5 days, p = 0.02) and hospital stays (20.5 +/- 17 vs 7.9 +/- 5.0 days, p = 0.05). In conclusion, MVAs are common in acute RV infarctions. They frequently occur before reperfusion and are associated with larger infarcts. With reperfusion, MVAs had little impact on intensive care and hospital stays or in-hospital mortality, except in patients with electrical storm.

Predictive Factors of Regional Toxicity and Serum Creatine Phosphokinase Levels After Isolated Limb Infusion for Melanoma: A Multi-Institutional Analysis

Isolated limb infusion (ILI) is a minimally invasive technique delivering regional chemotherapy to treat in-transit extremity melanoma. Determining perioperative factors that could predict toxicity is important to optimize strategies to improve clinical outcomes after regional chemotherapy in melanoma. Perioperative factors from 171 ILI patients performed at eight centers from 2001 to 2008 were reviewed. The Wieberdink limb toxicity scale and creatine phosphokinase (CK) levels were used to measure toxicity. Logistic regression analysis was used to estimate the association between toxicity and perioperative parameters. Mild (grades I-II) and severe (grades >or=III) limb toxicity developed in 68% and 32% of patients, respectively. Melphalan adjusted for ideal body weight (aIBW) and papaverine were used in 47% and 63% of patients, respectively. Median peak CK for all patients was 563 U/l, and median peak occurred at postoperative day 4. On univariate analysis, papaverine and high CK levels (>563 U/l) were significantly associated with higher toxicity. On the contrary, aIBW was significantly associated with a lower risk of severe toxicity. Perfusate blood gas at 30 min [pH, PaO(2), and base excess (BE) ], limb temperature, and ischemia time were not predictive of limb toxicity. On multivariate analysis, severe toxicity was associated with female sex (P = 0.01), papaverine (P = 0.01), and high peak CK levels (P < 0.01). Independent predictors of high CK levels included younger age, unadjusted melphalan dose, and low PaO(2) at 30 min. ILI can be performed with an acceptable morbidity. Papaverine use, female gender, and high peak CK were associated with higher limb toxicity. CK levels can be diminished significantly with aIBW.

Plasma homocysteine level and left ventricular thrombus formation in acute anterior myocardial infarction patients following thrombolytic therapy with t-PA

Aims The aim of this study was to evaluate the relationship between homocysteine levels and the development of left ventricular thrombus in acute anterior myocardial infarction patients directed to thrombolytic therapy. Methods and Results Seventy-nine patients presenting with ST elevated acute anterior myocardial infarction and treated with thrombolytic agent, t-PA, were included in the study. Two-dimensional echocardiography was used to divide patients into 2 groups according to the presence (n = 14) or absence (n = 65) of thrombus in the left ventricle following myocardial infarction. The levels of fasting plasma total homocysteine, total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, vitamin B12 and folic acid were assessed. There were no significant differences between two groups in terms of age, gender, hyperlipidemia and smoking. History of diabetes mellitus (28.57% versus 6.15%, p = 0.04), peak creatine phosphokinase levels (4153.54 ± 1228.41 U/L versus 2456.92 ± 1421.36 U/L, p < 0.001), mean left ventricular wall motion score index (2.21 ± 0.18 versus 1.83 ± 0.23, p < 0.001) and total fasting homocysteine levels (18.24 ± 5.67 mmol/L versus 12.31 ± 3.52 mmol/L, p < 0.001) were significantly higher in patients with left ventricular thrombus. In multivariate analysis; only diabetes mellitus (p = 0.03), higher wall motion score index (p = 0.001) and higher homocysteine levels (p = 0.04) were independent predictors of left ventricular thrombus formation. Conclusion Our results suggest that; diabetes mellitus, higher wall motion score index and hyperhomocysteinemia independently increases the risk for the development of left ventricular thrombus formation in patients with acute anterior myocardial infarction following thrombolytic therapy.

JDSA JOURNAL ABSTRACTS

JDSA JOURNAL ABSTRACTS

Comparison of Myocardial Reperfusion in Patients With Fasting Blood Glucose ≤100, 101 to 125, and >125 mg/dl and ST-Elevation Myocardial Infarction With Percutaneous Coronary Intervention

Diabetes and impaired fasting glucose (FG) were associated with worse outcomes in patients with acute myocardial infarction (MI). Because the underlying mechanism is not entirely clear, 376 consecutive patients with ST-elevation MI who underwent primary percutaneous coronary intervention (PPCI) were investigated. Patients were divided into 3 groups based on FG < or =100, FG of 101 to 125, and FG >125 mg/dl or previously diagnosed diabetes mellitus (DM) and studied for electrocardiographic signs of myocardial reperfusion (both spontaneous and after PPCI) and clinical outcomes. Clinical reperfusion was less likely with increasing FG: FG < or =100 mg/dl, 26%; FG of 101 to 125, 19%; and FG >125 and/or DM, 16% (p for trend = 0.03). Accordingly, angiographic TIMI grade 3 flow on initial angiography was 22% for FG < or =100 mg/dl, 13% for FG of 101 to 125, and 14% for FG >125 and/or DM (p for trend = 0.05). Despite similar TIMI flow after PPCI, early ST-segment resolution (> or =70%) was noted in 76%, 63%, and 60% in patients with FG < or =100 mg/dl, FG of 101 to 125, and FG >125 and/or DM, respectively (p for trend <0.01). Peak creatine phosphokinase (CPK) increased gradually, whereas left ventricular ejection fraction decreased with increased FG. Worse outcomes were observed with increasingly higher FG for heart failure (9%, 23%, and 26%; p for trend <0.01), cardiogenic shock (5%, 7%, and 13%; p for trend = 0.02), in-hospital mortality (1%, 2%, and 6%; p for trend = 0.01), and long-term mortality (2.5%, 4.5%, and 12%; p for trend <0.01) for patients with FG < or =100 mg/dl, FG of 101 to 125, and FG >125 and/or DM, respectively. In conclusion, increased FG and previously diagnosed DM were associated with less spontaneous reperfusion and less myocardial reperfusion after PPCI, resulting in worse clinical outcomes.

Association of TIMI Myocardial Perfusion Grade and ST-segment resolution with cardiovascular magnetic resonance measures of microvascular obstruction and infarct size following ST-segment elevation myocardial infarction

Impairment of coronary microvascular perfusion is common among patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). Cardiovascular magnetic resonance imaging (CMR) can identify microvascular obstruction (MO) following reperfusion of STEMI. We hypothesized that myocardial perfusion, as assessed by the Thrombolysis in Myocardial Infarction (TIMI) Myocardial Perfusion Grade (TMPG), would be associated with a CMR metric of MO in this population. Twenty-one STEMI patients who underwent successful primary PCI were evaluated. Contrast-enhanced CMR was performed within 7 days of presentation and repeated at three months. TIMI Flow Grade (TFG), corrected TIMI Frame Count (cTFC), TMPG, MO, infarct size, and left ventricular ejection fraction (EF) were assessed. The median peak creatine phosphokinase (CPK) was 1,775 IU/l (interquartile range 838-3,321). TFG 3 was present following PCI in 19 (90%) patients. CMR evidence of MO was present in 52% following PCI. Abnormal post-PCI TMPG (0/1/2) was present in 48% of subjects and was associated with MO on CMR (90% MO with TMPG 0/1/2 vs. 18% MO with TMPG 3, P < 0.01). Abnormal post-PCI TMPG was also associated with a greater peak CK (median 3,623 IU/l vs. 838 IU/l, P < 0.001) and greater relative infarct size (17.3% vs. 5.2%, P < 0.01). Among STEMI patients undergoing primary PCI, post-PCI TMPG correlates with CMR measures of MO and infarct size. The combined use of both metrics in a comprehensive assessment of microvascular integrity and infarct size following STEMI may aid in the evaluation of future therapeutic strategies.