Increase In CK-MB Research Articles

Usefulness of Colchicine to Reduce Perioperative Myocardial Damage in Patients Who Underwent On-Pump Coronary Artery Bypass Grafting

The objective of the present study was to test whether a perioperative course of colchicine, in patients who underwent standard coronary artery bypass grafting, would result in reduced postoperative increase of myocardial injury biomarker levels. Patients were prospectively randomized to colchicine or placebo starting 48 hours before scheduled coronary artery bypass grafting and for 8 days thereafter (0.5 mg twice daily). The primary outcome parameter was maximal high-sensitivity troponin T (hsTnT) concentration within 48 hours after surgery. Secondary outcome measures were maximal creatine kinase-myocardial brain fraction (CK-MB) levels and area under the curve (AUC) of hsTnT and CK-MB concentrations; 59 patients were included. Maximal hsTnT was 616 pg/ml (396 to 986) in the colchicine group versus 1,613 pg/ml (732 to 2,587) in controls (p = 0.002). Maximal CK-MB was 44.6 ng/ml (36.6 to 68.8) and 93.0 ng/ml (48.0 to 182.3), respectively (p = 0.002). The median AUC for hsTnT was 40,755 pg h/ml (20,868 to 79,176) in controls versus 20,363 pg h/ml (13,891 to 31,661) in the colchicine group (p = 0.002). AUCs for CK-MB were 2,552 ng h/ml (1,564 to 4,791) in controls and 1,586 ng h/ml (1,159 to 2,073) in the colchicine group (p = 0.003). The main complaints associated with colchicine were, as expected, gastrointestinal, with 5 patients (16.7%) in the colchicine group reporting diarrhea versus 1 control (3.4%) (p = 0.195). In conclusion, a short perioperative course of colchicine was effective in attenuating postoperative increases of hsTnT and CK-MB compared with placebo. This finding, which needs confirmation in a larger clinical trial powered to assess clinical endpoints, suggests a potential role for this agent in reducing cardiac surgery-related myocardial damage.

Homocysteine and risk of periprocedural myocardial infarction in patients undergoing coronary stenting

Despite improvements in pharmacological and mechanical devices, the risk of periprocedural myocardial infarction (PMI) is still high, particularly in prothrombotic conditions. Hyperhomocysteinemia has been associated with enhanced platelet function, impaired endothelial function and prothrombotic status, thus increasing the risk of cardiovascular events. No study has, so far, investigated the relationship between homocysteine levels and the risk of periprocedural MI in patients undergoing percutaneous coronary intervention (PCI), and this is therefore the aim of the current study. In 1150 patients undergoing PCI, homocysteinemia was assessed at admission. Cardiac biomarkers were measured at intervals from 8 to 48 h after PCI. Periprocedural myonecrosis was defined by a troponin I increase to three times the upper limit of normal (ULN) or by 50% if elevated at the time of the procedure. PMI was defined as a CK-MB increase to three times the ULN or of 50% if elevated at the time of the procedure. We grouped patients according to tertile values of homocysteine. Higher homocysteine levels were associated with older age (P < 0.001), male sex (P = 0.02), arterial hypertension (P = 0.007), diabetes (P = 0.04), renal failure (P < 0.001), higher creatinine levels (P = 0.01), previous MI (P = 0.02), previous PCI (P = 0.04) and previous cerebrovascular accidents (P = 0.01). Homocysteine was associated with lower ejection fraction (P < 0.001), treatment with angiotensin-receptor blockers (P < 0.001), nitrates (P = 0.008) and diuretics (P < 0.001) and acetylsalicylic acid (P = 0.01). Homocysteine levels were directly related with the extent of coronary disease (P = 0.04) and coronary calcifications (P < 0.001) but inversely with type C lesions (P = 0.001), TIMI 3 flow pre-PCI (P = 0.02), stenosis severity (P = 0.01) and thrombus (P = 0.004). In addition, they are associated with higher rates of balloon predilatation (P = 0.02), lower use of thrombectomy (P = 0.01) and periprocedural administration of GPIIbIIIa inhibitors (P = 0.02). Ageing, male sex, diabetes, renal failure, creatinine levels, diuretics use, coronary calcifications and type C lesions were independently related to homocysteine. Homocysteine did not affect the risk of PMI [adjusted odds ratio (OR) 1.14 (0.91-1.42), P = 0.26], or periprocedural myonecrosis [adjusted OR 1.17 (0.98-1.39), P = 0.08]. Similar results were found after propensity score adjustment [adjusted OR 1.19 (0.95-1.48), P = 0.14 for PMI and adjusted OR 1.18 (0.99-1.4), P = 0.07 for myonecrosis] and at subgroup analysis in higher risk subsets of patients. In patients undergoing PCI, the risk of PMI is not influenced by hyperhomocysteinemia.

Effect of short-term high-dose atorvastatin on systemic inflammatory response and myocardial ischemic injury in patients with unstable angina pectoris undergoing percutaneous coronary intervention

Background Percutaneous coronary intervention (PCI) could develop periprocedural myocardial infarction and inflammatory response and statins can modify inflammatory responses property. The aim of this study was to evaluate whether short-term high-dose atorvastatin therapy can reduce inflammatory response and myocardial ischemic injury elicited by PCI. Methods From March 2012 to May 2014, one hundred and sixty-five statin-naive patients with unstable angina referred for PCI at Department of Cardiology of the 306th Hospital, were enrolled and randomized to 7-day pretreatment with atorvastatin 80 mg/d as high dose group (HD group, n=56) or 20 mg/d as normal dose group (ND group, n=57) or an additional single high loading dose (80 mg) followed 6-day atorvastatin 20 mg/d as loading dose group (LD group, n=52). Plasma C-reactive protein (CRP) and interleukin-6 (IL-6) levels were determined before intervention and at 5 minutes, 24 hours, 48 hours, 72 hours, and 7 days after intervention. Creatine kinase-myocardial isoenzyme (CK-MB) and cardiac troponin I (cTnI) were measured at baseline and then 24 hours following PCI. Results Plasma CRP and IL-6 levels increased from baseline after PCI in all groups. CRP reached a maximum at 48 hours and IL-6 level reached a maximum at 24 hours after PCI. Plasma CRP levels at 24 hours after PCI were significantly lower in the HD group ((9.14±3.02) mg/L) than in the LD group ((11.06±3.06) mg/L) and ND group ((12.36±3.08) mg/L, P &lt;0.01); this effect persisted for 72 hours. IL-6 levels at 24 hours and 48 hours showed a statistically significant decrease in the HD group ((16.19±5.39) ng/L and (14.26±4.12) ng/L, respectively)) than in the LD group ((19.26±6.34) ng/L and (16.03±4.08) ng/L, respectively, both P &lt;0.05) and ND group ((22.24±6.98) ng/L and (17.24±4.84) ng/L, respectively). IL-6 levels at 72 hours and 7 days showed no statistically significant difference among the study groups. Although PCI caused a significant increase in CK-MB and cTnI at 24 hours after the procedure in all groups, the elevated CK-MB and cTnI values were lower in the HD group ((4.71±4.34) ng/ml and (0.086±0.081) ng/ml, respectively) than in the ND group ((7.24±6.03) ng/ml and (0.138±0.103) ng/ml, respectively, both P &lt;0.01) and LD group ((6.80±5.53) ng/ml and (0.126±0.101) ng/ml, respectively, both P &lt;0.01). Conclusion Short-term high-dose atorvastatin treatment before PCI significantly reduced systemic inflammatory response and myocardial ischemic injury elicited by PCI.

Impact on prognosis of periprocedural myocardial infarction after percutaneous coronary intervention.

Different definitions of periprocedural myocardial infarction (MI) after percutaneous coronary intervention (PCI) have been provided, but their impact on prognosis remains to be determined. Procedural data from consecutive patients undergoing PCI from 2009 to 2011 were revised to adjudicate diagnosis of periprocedural MI according to CK-MB increase (>3 × URL and >5 × URL), to troponin increase (>3 × 99th percentile URL and >5 × 99th percentile URL) and to recent 2012 Task Force and Society for Cardiovascular Angiography and Interventions (SCAI) definitions. Major adverse cardiovascular events (MACE) was the primary end-point. Seven hundred twelve patients were enrolled; after 771 days, 115 (16.7%) patients experienced MACE. One hundred ninety patients were diagnosed with a periprocedural MI defined as elevation of troponin >5 × 99th percentile of URL. When adjudicating 2012 Task Force definition on these patients, 46 were excluded and 1.4% of them experienced a MACE and 0.3% died, while among 144 with periprocedural MI, 2.9% reported a MACE and 1.3% died. After appraisal of SCAI definition, 176 patients were excluded, 3.8% of them with a MACE and 1.4% died, and for those with periprocedural MI, 0.5% experienced a MACE and 0.1% died. Similar low performance was appraised after reclassification of patients from more than 3 of upper limit of CK-MB and of troponin. At multivariate analysis, none of these definitions related to adverse events. Periprocedural MI represents a frequent complication for patients undergoing PCI. All present definitions share a still not satisfactory discrimination between patients with and without adverse events at follow-up, stressing the need for more accurate definitions.

Eosinophils count and periprocedural myocardial infarction in patients undergoing percutaneous coronary interventions

BackgroundEosinophils have been involved in a wide spectrum of pro-inflammatory and pro-thrombotic conditions, with the development of cardiovascular complications in a significant proportion of hypereosinophilic patients. However, no study has so far evaluated the impact of eosinophils levels on periprocedural myocardial infarction (PMI) in patients undergoing non-urgent percutaneous coronary interventions (PCI), that was, then, aim of current study. MethodsIn a consecutive cohort of patients, myonecrosis biomarkers were dosed at intervals from 6 to 48 h after PCI. Periprocedural myonecrosis was defined as troponin I increase by 3 times the ULN or by 50% of an elevated baseline value, whereas PMI as CKMB increase by 3 times the ULN or 50% of baseline. ResultsOur population is represented by 1543 patients who were divided according to tertiles of absolute eosinophils count (AEC ≤ 0.1; 0.1–0.2; >0.2 × 10ˆ3/ml). Higher AEC was related to male gender (p = 0.002), arterial hypertension (p = 0.02), diabetes (p = 0.001), previous coronary revascularization (p = 0.003 for PCI, p = 0.03 for CABG), treatment with ARBs, beta-blockers, diuretics and ASA (p < 0.001), statins (p = 0.02), calcium antagonists (p = 0.05), glycosylated hemoglobin (p < 0001), creatinine levels (p = 0.001) and platelet count (p = 0.01), while inversely with acute presentation (p < 0.001), glycemia (p = 0.03), HDL-cholesterol and C-reactive protein (p = 0.02). AEC related with multivessel coronary artery disease (p = 0.05), lesion length (p = 0.01), drug eluting stents implantation (p = 0.001) and use of kissing balloon technique (p = 0.05), while inversely to intracoronary thrombus (p < 0.001) and thrombectomy (p = 0.04).AEC did not influence the occurrence of PMI (p = 0.06, adjusted OR [95% CI] = 1.06 [0.86–1.31], p = 0.57) or myonecrosis (p = 0.15, adjusted OR [95% CI] = 1.06 [0.88–1.27], p = 0.53). Results were confirmed at subgroup analysis in higher-risk subsets of patients. ConclusionIn patients undergoing non-urgent PCI, eosinophils levels are not associated with the occurrence of periprocedural myocardial infarction or myonecrosis.

Curcumin Treatment Protects Against Renal Ischemia and Reperfusion Injury–Induced Cardiac Dysfunction and Myocardial Injury

ObjectivesRenal ischemia and reperfusion (I/R) injury frequently leads to acute renal failure (ARF) and multiple-organ injury with a substantial morbidity rate. The primary cause of ARF-associated death is, however, cardiac failure instead of renal failure itself, and the pathogenesis of renal I/R-induced cardiac injury is still poorly understood. We evaluated the efficacy of curcumin pretreatment on cardioprotection. MethodsThirty Sprague-Dawley rats were evenly divided into 3 groups of sham-operated control, renal I/R injury, and a curcumin pretreatment group. Renal ischemia was conducted by bilateral occlusions of pedicles for 45 minutes, followed by 3 hours of reperfusion. The cardiac function was assessed by the left ventricular end-systolic-pressure-volume-relation (ESPVR), systolic pressure (SP), ejection fraction (EF), and stroke volume (SV). Myocardial injury was assessed based on creatine kinase muscle brain fraction (CK-MB) and Troponin I (cTnI), and kidney injury was assessed based on blood urea nitrogen (BUN) and creatinine. We also assessed the levels of tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) in the heart tissues. ResultsSV, EF, and SP reduced moderately during the ischemic phase with no major change in ESPVR. During reperfusion, SV, SP, and ESPVR initially increased, and then steadily decreased. Myocardial and kidney injury were marked by the increases in serum CK-MB and cTnI, and creatinine and BUN level. Curcumin pretreatment ameliorated ESPVR and attenuated injuries of both the heart and kidney resulting from I/R insult. ConclusionsCurcumin pretreatment improved cardiac contractility and attenuated myocardial and renal injury through reducing inflammatory response in the kidney and heart and oxidative stress in the myocardium.

MTHFR polymorphism and risk of periprocedural myocardial infarction after coronary stenting

Background and aimPro-thrombotic status and platelet hyperreactivity still represent an important challenge for periprocedural myocardial infarction (PMI) after coronary stenting. Hyperhomocysteinemia has been suggested to increase the risk of cardiovascular events. The genetic variant of methylenetetrahydrofolate reductase (MTHFR) 677 C > T has been associated to reduced function of the enzyme, thus inducing hyperhomocysteinemia. In our study we investigated whether MTHFR 677 C > T polymorphism is associated with increased risk of periprocedural MI in patients undergoing coronary stenting. Methods and resultsWe included 778 patients undergoing PCI. Homocysteinemia and genetic status were assessed at admission for all patients. Myonecrosis biomarkers were dosed at intervals from 6 to 48 h, PMI was defined as CKMB increase by 3 times the ULN or 50% of pre-PCI value, periprocedural myonecrosis for troponin I increase by 3 times the ULN or by 50% of the baseline. As many as 521 patients carried the MTHFR-T allele. No difference was found for main demographical and clinical features nor for biochemistry parameters, but for higher rate of statins treatment (p = 0.03) in T-carriers. Polymorphic patients displayed significantly higher levels of homocysteine (p = 0.005), with additive effect of the mutated T-alleles. Angiographic and procedural features were similar according to genetic status.MTHFR677T was not associated with periprocedural myocardial infarction (adjusted OR = 0.97[0.67–1.4], p = 0.87) or myonecrosis (adjusted OR = 1.03[0.83–1.36], p = 0.82). Same results were found at subgroup analysis in higher-risk subsets of patients. ConclusionOur study showed that among patients undergoing PCI, MTHFR 677 C > T polymorphism is associated to higher homocysteine levels, but does not influence the risk of periprocedural myocardial infarction.

Association of baseline C‐reactive protein levels with periprocedural myocardial injury in patients undergoing percutaneous bifurcation intervention: A CACTUS study subanalysis

To assess the predictive value of C-reactive protein (CRP) on periprocedural myocardial injury (PMI), evaluated by creatine kinase-myocardial band isoform (CK-MB) elevation in patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stent (DES) implantation for the treatment of coronary bifurcation lesions is actually unknown. Systemic inflammation as assessed by CRP has been associated with averse events after DES implantation. After PCI, the occurrence of PMI is common and has also been associated with worse outcomes. Finally, bifurcations are frequently encountered anatomically complex lesions which the treatment is associated with higher complication rate compared with simple lesions. A total of 96 patients (66 ± 10 years, 70 men) from the Coronary bifurcations: Application of the Crushing Technique Using Sirolimus-eluting stents (CACTUS) trial who had baseline CRP dosage and both baseline and postprocedural CK-MB measurement were included. A complex bifurcation strategy was implemented in 53 (55%) patients, and angiographic success was achieved in all but two (2%) patients. Periprocedural myocardial necrosis (increase of CK-MB between one and three times the upper limit of normal [ULN]) was observed in 12 (13%) patients, and four (4%) patients had PCI-related myocardial infarction (increase of CK-MB more than three times ULN). Notably, progressively higher CRP levels were observed in patients with different increase in CK-MB (P = 0.041). Moreover, CRP >1 mg/L significantly predicted CK-MB rise (odds ratio 5.6, 95% confidence interval 1.5-4.3, P = 0.011). In the setting of true coronary bifurcations treated by DES, baseline CRP levels were significantly associated with both the incidence and the extent of PMI.

Is no‐no‐reflow following PCI in AMI due to distal embolization of plaque and thrombus?

Catheterization and Cardiovascular Interventions 82:210–211 (2013) Editorial Comment Is no-no-reflow following PCI in AMI due to distal embolization of plaque and thrombus? Jonathan Tobis,* MD Director of Interventional Cardiology, Prof. of Medicine, Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California Of 3400 patients enrolled in the Horizons-AMI (acute myocardial infarction) trial that assessed the use of bivalirudin versus heparin plus routine GP IIb/IIIa inhibition, 402 patients had intravascular ultrasound (IVUS) imaging poststenting, and of these, 43 patients had IVUS imaging before any intervention as well as post stenting. The accompanying paper [1] describes the observations in this final select group of patients. The authors conclude: 1. In addition to the artery lumen enlarging from the stent, there was a decrease in lesion segment plaque volume. The decrease in plaque volume was greater than the shift of plaque longitudinally from the lesion to the proximal and distal references. 2. The decrease in lesion plaque volume was greater in patients with angiographic thrombus compared to those with no angiographic thrombus. 3. The post-intervention CK-MB correlated with the reduction in plaque volume. This article represents a large amount of meticulous work, measurements and analysis, not only on this subset of patients but also for the larger IVUS cohort and for the multicenter Horizons- AMI trial. The authors should be congratulated because it is difficult to obtain these data. Of the 43 patients who had an acute MI and had IVUS imaging prestenting and poststenting, 20 had thrombus identified by angiography and 23 did not. None of the patients with thrombus received thrombectomy. There was more loss of plaque volume in pts with thrombus versus those without thrombus. five patients with thrombus had no-reflow but none of the patients without thrombus had no-reflow. It is a bit difficult to draw emphatic conclusions with such small numbers of patients, but it certainly is consistent with the hypothesis that percutaneous coronary intervention (PCI) with stenting breaks up thrombus which then heads downstream and causes no-reflow. The periprocedural increase in CK-MB correlated with the reduction in plaque volume which also is suggestive that PCI can release material downstream and cause myocardial necrosis, especially if thrombus is present. So why are there such ambiguous results with thrombectomy in AMI? The authors conclude: “The current findings may also explain why thrombus aspiration or distal protection is not universally beneficial since not all patients with AMI have thrombus,” as documented in this study with IVUS. Perhaps the identification of thrombus would be more sensitive with OCT imaging, but I believe that IVUS is accurate for quantifying a large intralumenal mass of thrombus.

Platelet distribution width and the risk of periprocedural myocardial infarction in patients undergoing percutaneous coronary intervention

Periprocedural myocardial infarction (PMI) still occurs in a large amount of percutaneous coronary interventions (PCI), mainly due to increased platelet activation. Platelet size has been suggested as an indicator of enhanced reactivity and platelet distribution width (PDW) could reflect morphologic changes in platelets, therefore affecting their function and potentially increasing the risk of complications after coronary stenting. Aim of the present study was to evaluate the relationship between PDW and PMI. We included 1,300 consecutive patients undergoing PCI. Myonecrosis biomarkers were dosed at intervals from 6 to 48h after PCI. Periprocedural myonecrosis was defined as troponin I increase by three times the ULN or by 50% of an elevated baseline value, whereas PMI as CKMB increase by three times the ULN or 50% of baseline. We grouped patients according to tertiles values of PDW (<12.1; ≥13.9). Higher PDW was associated with age (p=0.03), diabetes (p<0.001), previous cerebrovascular accidents (p=0.04), therapy with statins (p=0.001) and ARBs (p<0.001), ASA (p=0.02), nitrates (p=0.006), calcium antagonists (p=0.05) and lower pre-procedural clopidogrel bolus (p=0.005). PDW related with haemoglobin levels (p<0.001), while inversely to platelet count (p<0.001) and glycaemia (p=0.003). Patients with larger PDW had lower presence of coronary thrombus (p<0.001), higher rate of coronary calcifications (p=0.02), higher stenting rate (p=0.03) and lower rate of distal embolization (p=0.03). Larger PDW did not increase risk of PMI (p=0.11; adjusted OR [95% CI]=0.94 [0.78-1.1], p=0.55) or periprocedural myonecrosis (p=0.73; adjusted OR [95% CI]=0.95 [0.82-1.1], p=0.51). Results were confirmed even in higher-risk subgroups of patients. In patients undergoing coronary stenting, PDW does not increase the risk of periprocedural MI and therefore should not be considered a risk factor for thrombotic periprocedural complications after PCI.

Routine early versus deferred provisional tirofiban treatment in patients with acute coronary syndrome undergoing percutaneous coronary intervention

The present study examined the optimal timing of tirofiban administration in moderate- or high-risk non-ST segment elevated acute coronary syndrome (NSTE-ACS) patients undergoing percutaneous coronary intervention (PCI). Eligible patients were randomized into two groups. Tirofiban was administered routinely at ≥4h before angiography (routine early group; n=141 patients) or provisionally only for bailout after angiography (deferred provisional group; n=145 patients). The parameters analysed were: creatine kinase MB isoenzyme (CK-MB), thrombolysis in myocardial infarction (TIMI) flow, thrombotic complications during PCI, efficacy end-points (death, myocardial infarction or target vessel revascularization) at 7, 30 and 180days and safety end-points (bleeding or thrombocytopenia). In the deferred provisional group, 48 patients (33.1%) required bailout tirofiban. Tirofiban was administered 5.8h earlier in the routine early compared with the deferred provisional group. The routine early group showed a lower percentage increase in CK-MB (in U/L) 12-24h after PCI compared with the deferred provisional group (0 (-4.0, 3.0) vs 0.4 (-3.0, 5.0), respectively; P=0.045), as well as higher pre-PCI TIMI 3 (i.e. normal) flow (78.7% vs 64.8%, respectively; P=0.042) and a lower incidence of thrombotic events (5.0% vs 33.1%, respectively; P<0.0001). There were no significant differences in efficacy and safety end-points. In patients with moderate- or high-risk NSTE-ACS, early tirofiban combined with dual antiplatelet therapy was associated with better patency before PCI, attenuated minor myocardial damage and a lower prevalence of thrombotic complications during PCI, but had no significant benefit on the post-PCI TIMI 3 flow or short-term prognosis.

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Prevalence and Effect of Myocardial Injury After Transcatheter Aortic Valve Replacement

The incidence and prognostic implication of myocardial injury after transcatheter aortic valve replacement (TAVR) have not been consistently studied. We aimed to assess the incidence and extent of myocardial injury after TAVR performed using transfemoral and transapical approaches. The clinical data from patients with aortic stenosis who underwent TAVR were retrospectively analyzed. The myocardial necrosis markers cardiac troponin I and creatine kinase (CK)-MB were assessed during hospitalization. Of the 150 TAVR patients, 95% and 50% had an abnormally elevated cardiac troponin I and CK-MB level, respectively. The transapical patients had significantly greater elevations of both cardiac troponin I (13.8 ± 14.0 vs 2.5 ± 5.8 ng/ml, p <0.001) and CK-MB (28.4 ± 24.2 vs 7.4 ± 8.6 ng/ml, p ≤0.001). On receiver operating curve analysis, postprocedural CK-MB (twofold increase) had high predictive power for 30-day mortality (area under the curve 0.85, p <0.001). Patients with high CK-MB levels had greater rates of postprocedural kidney injury (22% vs 6%, p = 0.026), in-hospital (22% vs 0%, p <0.001), 30-day (27% vs 1.5%, p <0.001), and 1-year mortality (41% vs 18%, p = 0.01). Baseline renal failure and no β-blocker treatment on admission were independent predictors of an elevated postprocedural CK-MB level. In conclusion, a cardiac biomarker increase after TAVR was common and more frequent among transapical access patients. A twofold increase (>7 ng/ml) in CK-MB after transfemoral TAVR was a surrogate for poor long-term outcomes.

Mean platelet volume and the risk of periprocedural myocardial infarction in patients undergoing coronary angioplasty

BackgroundPeriprocedural myocardial infarction (PMI) represents a relatively common complication of percutaneous coronary intervention (PCI). Mean platelet volume (MPV) has been proposed as a marker for platelet activation, as larger sized platelets have been associated with higher pro-thrombotic risk. Therefore, aim of the current study was to evaluate whether MPV is associated with increased risk of PMI after PCI. MethodsWe included 1056 consecutive patients undergoing PCI. We measured myonecrosis biomarkers at intervals from 6 to 48 h after PCI. Periprocedural myonecrosis was defined for troponin I increase by 3 times the ULN or by 50% if elevated at the time of the procedure. PMI was defined as CK-MB increase by 3 times the ULN or 50% if elevated at the time of the procedure. ResultsWe grouped patients according to tertiles values of MPV (<10.4 fl; 10.5–11.3 fl; >11.4 fl). High MPV was associated with diabetes (p = 0.025) and higher prevalence of cerebrovascular events (p = 0.005). MPV significantly related with haemoglobin levels (p < 0.001), but inversely to platelet count (p < 0.001) and higher presence of thrombus (p = 0.03). Larger sized platelets did not increase risk of periprocedural myonecrosis (p = 0.91; OR[95% CI] = 1.04[0.90–1.2], p = 0.64) or PMI (p = 0.09; OR[95%IC] = 1.13[0.93–1.37]; p = 0.20). Subgroup analysis confirmed no impact of MPV on periprocedural MI also in high-risk subsets of patients, such as those with ACS at presentation (OR[95%CI] = 1.09 [0.87–1.38]; p = 0.44), diabetes (OR[95% CI] = 1.02[0.71–1.47], p = 0.91), female gender (OR [95% CI] = 1.15 [0.78–1.71], p = 0.48), elderly patients (age ≥ 75 years) (OR[95%CI] = 1.21[0.87–1.69], p = 0.25) or with renal failure (OR[95%CI] = 1.55[0.91–2.61], p = 0.1). ConclusionsThis study demonstrates that MPV does not predict the risk of PMI in patients undergoing PCI.

Source, Triggers and Clinical Implications of Hyperlactemia in Patients Undergoing Mitral Valve Surgery Using Custodiol Cardioplegia

Background: Postoperative blood hyperlactaemia is an indicator of organ anaerobic metabolism and is associated with morbidity after cardiac surgery. This prospective study aims to explore the source, triggers and clinical implications for hyperlactaemia in patients undergoing mitral valve surgery using Custodiol cardioplegia. Methods: Twenty consecutive elective patients undergoing open-heart surgery for mitral valve repair/replacement using Custodiol (based on Bretschneider’s HTK-solution) cardioplegia were recruited. A serial measurement of arterial blood lactate was performed. Pre-, intra-and post-operative clinical data were obtained and cardiac injury was determined by serial plasma measurement of postoperative release of CK-MB. Results: There were no in-hospital deaths. Most of the patients (n = 16) needed intraoperative direct current cardioversion to treat ventricular arrhythmias or post-operative vasopressors (n = 13) to treat vasoplegia. There was significant cardiac injury as determined by the marked increase of serum CK-MB (p 0.05). A significant (p 0.05) increase in blood lactate was found to follow a biphasic profile. The first peak (from 0.54 ± 0.03 to 1.3 ± 0.07 mM) was observed immediately following the release of the aortic cross-clamp and remained high for 1 hour. This was followed by a second peak at 12 hours post-operatively (1.9 ± 0.2 mM). The second rise in lactate was seen only in patients that required post-operative vasopressors (1.3 ± 0.2 vs 2.2 ±0.3 mM, p 0.05), in whom a significant late decrease in CVP was also observed (12.2 ± 1.0 to 7.7 ± 1.0 for 1 and 12 hours postoperative, respectively). Hyperlactaemia did not correlate with any other variables including CK-MB levels, cross-clamp or cardiopulmonary bypass time. Conclusions: In patients undergoing mitral valve surgery with Custodiol cardioplegia there is marked cardiac injury and a biphasic release of blood lactate. The initial peak in lactate occurs immediately following unclamping the aorta and is likely to be of organ (e.g. heart and lungs) origin. A second peak is only seen in patients requiring postoperative vasopressors to treat vasoplegia. Hyperlactaemia following mitral valve surgery with Custodiol cardioplegia does not seem to be related to myocardial injury as expressed by CK-MB release.

CHANGES OF ELECTROCARDIOGRAM AND CK-MB IN THE PATIENTS WITH CEREBRO-CARDIAC SYNDROME CAUSED BY ACUTE CEREBRAL INFARCTION

ObjectivesTo investigate the changes of ECG activity and CK-MB in the patients with cerebro-cardiac syndrome caused by acute cerebral infarction and to analysis the relationship between ECG, CK-MB and the...

THE SERUM CONCENTRATIONS LEVEL OF CK, CK-MB AND CARDIAC TROPONIN T IN EARLY NEONATES WITH ASPHYXIA

Objective: Investigate the change of serum Creatine kinase (CK), CK-MB and cardiac troponin T concentrations in early neonates with asphyxia. The relation between the change of serum Creatine kinase (CK), CK-MB and cardiac troponin T concentrations and degree of asphyxia. The serum CK, CK-MB and cardiac troponin T concentrations of asphyxiated newborn were measured in the first 24 hours after admission. Material and methods: Patients: 27 early asphyxiated neonates with apgar mark at 5 minutes from 0-7.Study site: Neonatal of Pediatric department, Hue central hospital. Methods: Prospective, description study. Results: Asphyxiated neonates had significantly higher concentration of CK, CK-MB and Troponin T than controls: mean CK 1146.7±711.7U/L vs 145.6±26.4, p&lt;0.01; mean CK-MB 22.15±13.78ng/ml vs 2.77±1.08, p&lt;0.01; mean Troponin T 0.099±0.08ng/ml vs ≤0.01, p&lt;0.05. The serum CK, CK-MB and cardiac troponin T concentrations increased significantly with severity of asphyxia. Conclusion: There is an increase in CK, CK-MB and Troponin T levels in neonates with asphyxia. Correlation with statistical significance between the concentration of CK, CK-MB and troponin T with severity of asphyxia.

Troponin Criteria for Myocardial Infarction After Percutaneous Coronary Intervention

The universal definition of myocardial infarction specifies creatine kinase-MB fraction (CKMB) or troponin values more than 3 times the 99th percentile of the upper reference limit as diagnostic after percutaneous coronary intervention, with a preference for the use of troponin. Outcomes of 4930 patients with elective coronary stent placement between July 1, 2004, and September 30, 2007, as part of the EVENT (Evaluation of Drug Eluting Stents and Ischemic Events) registry were analyzed to test the association between 1-year mortality and postprocedure elevation of either CKMB or troponin. All values were normalized to the individual clinical center myocardial infarction diagnostic levels. Myocardial infarction occurred in 7.2% of patients by the CKMB criteria and in 24.3% of patients by the troponin criteria of greater than 3 times the diagnostic level. Both CKMB (hazard ratio [HR], 1.38; 95% CI, 1.22-1.55) and troponin (HR, 1.35; 95% CI, 1.18-1.54) as continuous values were associated with 1-year mortality. The mortality effect of a more than 3-fold increase was greater for CKMB (adjusted HR, 2.5; 95% CI, 1.5-4.1) than for troponin (adjusted HR, 1.7; 95% CI, 1.1-2.5). A troponin threshold more than 20 times the diagnostic level provided similar frequency (7.0%) and mortality risk (adjusted HR, 2.6; 95% CI, 1.6-4.3) as a 3-fold increase in CKMB. A regression spline model of the relationship between troponin and 1-year mortality demonstrated that the hazard of mortality increased from 1.02 at 3-fold to 1.67 at 20-fold troponin elevation. Troponin and CKMB elevations after percutaneous coronary intervention are associated with increased 1-year mortality rates, but thresholds for similar event frequency and mortality hazard are much higher for troponin than for CKMB.

Red Dry Wine Modulates Plasma Cholesterol Levels and Cardiac Enzymes in Humans

Several studies has pointed that red wine diet, rich in polyphenols, has several effects like vasodilation, possible antioxidant effect, decrease of cellular events of atherosclerosis, decrease of blood pressure, and reduction of cardiovascular risks. This paper proposes an investigation of the effects of a 21 days diet of 200 ml dialy of red dry wine for markers of muscle injury such as CK and CK-MB, besides cholesterol and its fractions, LDL and HDL, and triglycerides, in normal subjects.The results showeddecreased levels of plasma total cholesterol and LDL, and a tendency to increased levels of HDL, what suggests red dry wine has effects on decrease cardiovascular risks. However, significant increase of cardiacCK-MB isoenzyme was observed what could point to increase the oxidation of muscle tissues. It can be concluded that, despite the CK-MB increase, red dry wine can be considered as a tool to decrease cardiovascular diseases risks.

Effect of Statins on Creatine Kinase Levels Before and After a Marathon Run

We measured the serum levels of myoglobin, total creatine kinase (CK), and the CK myocardial (CK-MB), muscle (CK-MM), and brain (CK-BB) isoenzymes in 37 subjects treated with statins and 43 nonstatin-treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) and within 1 hour (FINISH) and 24 hours after (POST) the race. The hematocrit and hemoglobin values were used to adjust for changes in the plasma volume. The CK distribution was normalized using log transformation before analysis. The exercise-related increase in CK 24 hours after exercise, adjusted for changes in plasma volume, was greater in the statin users (PRE to POST 133 ± 15 to 1,104 ± 150 U/L) than in the controls (PRE to POST 125 ± 12 to 813 ± 137 U/L; p = 0.03 for comparison). The increase in CK-MB 24 hours after exercise was also greater in the statin users (PRE to POST 1.1 ± 3.9 to 8.9 ± 7.0 U/L) than in the controls (PRE to POST 0.0 ± 0.0 to 4.2 ± 5.0 U/L; p <0.05 for comparison). However, the increases in muscle myoglobin did not differ at any point between the 2 groups. Increases in CK at both FINISH and POST race measurements were directly related to age in the statin users (r(2) = 0.13 and r(2) = 0.14, respectively; p <0.05) but not in the controls (r(2) = 0.02 and r(2) = 0.00, respectively; p >0.42), suggesting that susceptibility to exercise-induced muscle injury with statins increases with age. In conclusion, our results show that statins increase exercise-related muscle injury.