Plasma intermedin levels in patients with acute myocardial infarction

It has been shown that adrenomedullin (ADM) may function as a cardiovascular-regulatory peptide in humans. Intermedin (IMD) is a newly discovered peptide related to ADM and has a greater range of biological effects on the cardiovascular in animal experiments. The purpose of the study was to investigate the pathophysiological role of IMD in patients with acute myocardial infarction (AMI). The present study included twenty patients with acute ST-segment elevation myocardial infarction (STEMI), thirty-three with stable coronary heart disease (SCHD), and eighteen healthy controls. Plasma levels of IMD, malonaldehyde (MDA), and superoxide dismutase (SOD) and cardiac biomarkers were determined at one, two, four and seven days following AMI. Plasma IMD levels were significantly increased on day 1 in AMI patients when compared with SCHD subjects (P = 0.014), and reached a peak of 181.88 ± 9.47 pg/ml at 96 h. Plasma IMD concentrations were correlated with MDA and SOD. Furthermore, patients with severe lesions in their coronary arteries tended to have higher plasma IMD levels (P < 0.05) in AMI patients. A significant increase in plasma IMD following AMI may be associated with oxidative stress, and could be used as a marker to reflect the severity of the coronary stenosis.     

Reciprocal change in ST segment in acute myocardial infarction: correlation with findings on exercise electrocardiography and coronary angiography.

The clinical relevance of reciprocal changes in the ST segment occurring at the time of acute myocardial infarction was studied prospectively in 85 consecutive uncomplicated cases. Reciprocal depression of the ST segment was defined as depression of 1 mm or more in electrocardiogram leads other than those reflecting the infarct. All patients underwent maximal, symptom limited treadmill stress testing two weeks after the infarct and coronary angiography six weeks after infarction. Forty six patients had inferior, 34 anterior, and five true posterior infarction. Of the 51 patients with reciprocal changes, 45 (88%) developed exercise induced ST segment depression in areas remote from the infarction zone. At angiography all 45 patients were shown to have stenoses greater than 70% in at least two major vessels. Four patients had negative exercise electrocardiograms and were sequently shown to have single vessel disease subtending their infarct, and the remaining two patients had a false negative treadmill test result. Of the 27 patients without reciprocal changes, 21 (78%) had negative treadmill stress test results associated with single vessel coronary disease. Five had positive stress test results and multivessel coronary disease, and one had a false negative stress test result. The remaining seven patients had ST segment elevation without Q wave formation in the reciprocal areas and were assessed separately. Of these, six had positive stress test results and multivessel coronary disease and one had a negative stress test result and single vessel coronary disease to the infarct area. Twenty one patients with anterior infarcts (62%) and 27 with inferior infarcts (59%) had reciprocal changes. No differences emerged in the relation between infarct site, reciprocal change, and presence of additional coronary disease. At follow up of the 51 patients with reciprocal changes in the ST segment 36 had become symptomatic, of whom 29 had undergone coronary artery bypass surgery. By contrast, only four of the 27 patients without reciprocal changes in the ST segment had developed symptoms, and two of these had undergone coronary revascularisation. Reciprocal ST segment depression at the time of acute myocardial infarction may identify patients with severe coronary disease who are at risk of subsequent cardiac events and appears to be as reliable as results of early postinfarction treadmill stress testing in predicting the underlying coronary anatomy. When the electrocardiogram does not show reciprocal changes treadmill testing provides valuable additional information.     

Decreased plasma nesfatin-1 levels in patients with acute myocardial infarction

Nesfatin-1 is a novel anorexigenic hormone which has close relationship with diabetes, obese, anorexia nervosa, psychiatric disorders and neurogenic diseases. The aim of our study was to evaluate levels of plasma nesfatin-1 among patients presenting with coronary artery disease and the correlation between nesfatin-1 levels and other clinical parameters. Fasting plasma levels of nesfatin-1 were tested in 48 acute myocardial infarction (AMI) patients, 74 stable angina pectoris (SAP) patients and 34 control subjects. All of them were examined by coronary angiography. The severity of coronary atherosclerosis was assessed using the Gensini score. Plasma nesfatin-1 levels were significantly lower in AMI group than SAP group or control group (0.91 ± 0.08 ng/mL vs. 0.98 ± 0.19 ng/mL and 1.09 ± 0.39 ng/mL, respectively, P < 0.05). In AMI patients, plasma nesfatin-1 levels were negatively correlated with high-sensitivity C-reactive protein, neutrophil% or Gensini scores. Such information implies that lower nesfatin-1 concentration may play a very important role in the development of AMI.     

Likelihood of coronary angiography among First Nations patients with acute myocardial infarction

Background:

Morbidity due to cardiovascular disease is high among First Nations people. The extent to which this may be related to the likelihood of coronary angiography is unclear. We examined the likelihood of coronary angiography after acute myocardial infarction (MI) among First Nations and non–First Nations patients.

Methods:

Our study included adults with incident acute MI between 1997 and 2008 in Alberta. We determined the likelihood of angiography among First Nations and non–First Nations patients, adjusted for important confounders, using the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease (APPROACH) database.

Results:

Of the 46 764 people with acute MI, 1043 (2.2%) were First Nations. First Nations patients were less likely to receive angiography within 1 day after acute MI (adjusted odds ratio [OR] 0.73, 95% confidence interval [CI] 0.62–0.87). Among First Nations and non–First Nations patients who underwent angiography (64.9%), there was no difference in the likelihood of percutaneous coronary intervention (PCI) (adjusted hazard ratio [HR] 0.92, 95% CI 0.83–1.02) or coronary artery bypass grafting (CABG) (adjusted HR 1.03, 95% CI 0.85–1.25). First Nations people had worse survival if they received medical management alone (adjusted HR 1.38, 95% CI 1.07–1.77) or if they underwent PCI (adjusted HR 1.38, 95% CI 1.06–1.80), whereas survival was similar among First Nations and non–First Nations patients who received CABG.

Interpretation:

First Nations people were less likely to undergo angiography after acute MI and experienced worse long-term survival compared with non–First Nations people. Efforts to improve access to angiography for First Nations people may improve outcomes.Although cardiovascular disease has been decreasing in Canada,¹ First Nations people have a disproportionate burden of the disease. First Nations people in Canada have a 2.5-fold higher prevalence of cardiovascular disease than non–First Nations people,² with hospital admissions for cardiovascular-related events also increasing.³The prevalence of cardiovascular disease in First Nations populations is presumed to be reflective of the prevalence of cardiovascular risk factors.^4–7 However, the disproportionate increase in rates of hospital admission suggests that suboptimal management of cardiovascular disease or its risk factors may also influence patient outcomes.^2,3 Racial disparities in the quality of cardiovascular care resulting in adverse outcomes have been documented, although most studies have focused on African-American, Hispanic and Asian populations.^8,9 As a result, it is unclear whether suboptimal delivery of guideline-recommended treatment contributes to increased cardiovascular morbidity and mortality among First Nations people.^10–12We undertook a population-based study involving adults with incident acute myocardial infarction (MI) to examine the receipt of guideline-recommended coronary angiography among First Nations and non–First Nations patients.^10–12 Among patients who underwent angiography, we sought to determine whether there were differences between First Nations and non–First Nations patients in the likelihood of revascularization and long-term survival.     

Prospective register of primary percutaneous coronary interventions in patients with acute myocardial infarction

The present study has evaluated the immediate angiographic results of primary percutaneous interventions (PCI) in patients with acute myocardial infarction, as well as hospital and 6-month clinical outcomes. The analysis covered a total of 265 patients (females (23%) and males (77%)); their mean age was 57+/-11 years. The mean time before the first balloon dilatation during PCI was 278+/-135 minutes after the development of the pain syndrome or 109+/-94 minutes after hospital admission. PCI proved to be effective in 96% of the patients, as evidenced by angiography. TIMI 3 blood flow was achieved in 83% of cases during PCI. After primary PCI, hospital mortality was 98.9% and 95% survived 6 months. At 6-month follow-up, 22% patients had positive exercise tests, recurrent angina pectoris and/or more than 50% luminal stenosis of the infarct-related artery. Control angiography made less than 6 months later showed 11% restenosis. This prospective study has demonstrated the high immediate and long effectiveness and safety of primary interventions in acute myocardial infarction.     

Antioxidant vitamin levels do not exhibit negative correlation with the extent of acute myocardial infarction

Serum levels of vitamin E (VE), beta-carotene (BC) and vitamin C (VC) were determined in 50 patients with the first acute myocardial infarction (AMI) before starting thrombolytical treatment. VE and BC were determined by HPLC, VC spectrophotometrically. The reperfused patients were divided according to vitamin concentrations into four groups. The lowest quartile was compared with the rest of the studied population (VE: group with high (H)>15.6 microM>group with low (L), BC: H>0.07 microM>L, VC: H>25 microM>L) in the following parameters: extent of myocardial damage (area under the curves of troponin I, CK-MB during 48 h), arrhythmia and congestive heart failure occurrence, size of ejection fraction, positivity of ventricular late potentials. No significant differences between groups H and L for either VE, BC or VC were found (P 0.05). As no correlation between serum concentrations of vitamins E, C and beta-carotene and the extent and clinical course of AMI was found, the actual vitamin concentrations may be important for prevention of ischemic heart a disease, but they do not play a decisive role in the acute phase of myocardial infarction in humans.     

Alterations in serum selenium levels and their relation to troponin I in acute myocardial infarction

Selenium (Se) is an essential trace element with antioxidant function. The aim of the present study was to estimate the alterations of Se serum level during the acute phase of myocardial infarction and its relation to biomarkers of myocardial necrosis. Serum Se levels were measured at admission and after 24 h in 60 consecutive patients with acute coronary syndrome (both with and without ST elevation). Troponin I (TnI) was assessed at admission and then twice daily for 3 days; patients with normal levels were excluded. Fifty-five patients with acute MI (positive TnI) were included into the analysis. During the first day of hospitalization, patients received standard therapy, including acetylsalicylic acid, clopidogrel, and heparin or enoxaparin; all underwent urgent coronary angiography and percutaneous intervention, when appropriate. Mean Se levels at baseline and 24 h later were comparable (67.1 ± 2.1 vs. 67.2 ± 1.8 μg/L, ns). Linear regression has shown significant correlation between baseline Se levels and peak TnI (y = 3.4x ? 116, r ² = 0.13, P = 0.008). Positive correlation was found also between the peak TnI and the difference from baseline to 24 h (y = 2.2x + 115, r ² = 0.08, P = 0.04). Moreover, close negative correlation was observed between baseline Se levels and the difference from baseline to 24 h (y = ?0.9x + 62.7, r ² = 0.55, P<0.001). Our results have shown marked individual changes in Se levels during the acute phase of MI as well as correlation between Se levels and peak TnI. These results suggest that alterations in serum Se may be related to the extent of myocardial infarction.     

Elevated serum YKL-40 levels in patients with Kawasaki disease

Context: YKL-40 is an inflammatory biomarker for endothelial dysfunction that may have a role in Kawasaki disease (KD).

Objectives: We investigated the association of serum YKL-40 levels with KD and established laboratory parameters for YKL-40 levels and other inflammatory markers.

Methods: YKL-40 levels and other inflammatory markers of 23 KD patients, 9 disease control patients and 11 age-matched healthy controls.

Results: YKL-40 concentration in the serum of KD patients significantly increased during the acute disease phase compared with those of disease controls and healthy controls.

Conclusions: Increased YKL-40 levels may provide a useful inflammatory marker for patients with KD.     

Elevated serum endothelin-1 levels in patients with colorectal cancer; relevance for prognosis

BACKGROUND: It has been demonstrated that the Doppler Perfusion Index (DPI) is increased in patients who are at risk of developing liver metastases from colorectal cancer. It has been postulated that a circulating hormonal factor is involved in the relative vasoconstriction throughout the splanchnic bed. Endothelin-1 (ET-1), a potent vasoconstrictor which has been associated with tumor growth and is produced by colorectal tumors, may play an important role in this phenomenon. In this paper the prognostic value of serum ET-1 in colorectal cancer is discussed. METHODS: Preoperative serum levels of ET-1 were assessed in three groups of patients: group A underwent resection of the colorectal tumor and remained free of recurrence (n=20); group B developed metachronous liver metastases at least six months after colorectal resection (n=14); and group C presented with colorectal cancer and synchronous liver metastases (n=22). RESULTS: The mean (SD) serum ET-1 levels in groups A, B and C were 1.59 (0.41) pmol/L, 1.70 (0.32) pmol/L and 1.85 (0.47) pmol/L, respectively. These values were significantly different from those of healthy controls (1.22 (0.31), p<0.05). Kaplan-Meier analyses revealed no prognostic value of preoperative serum ET-1 levels. CONCLUSIONS: These preliminary results demonstrate that serum ET-1 levels are raised in patients with colorectal cancer. Serum ET-1 levels do not seem to be of prognostic value for survival.     

Serum ghrelin levels in obese patients: the relationship to serum leptin levels and soluble leptin receptors levels

Ghrelin is a new endogenous ligand for the growth hormone secretagogue receptor. It activates the release of growth hormone from the pituitary and it also participates in the regulation of energy homeostasis. The aim of the study was to characterize changes in serum ghrelin levels in obese subjects and their relationship to the serum levels of leptin and soluble leptin receptor. Eight obese patients (6 women and 2 men) with body mass index (BMI) 40.3+/-13.4 kg.m(-2) and eight healthy controls (5 women and 3 men) with BMI 22.7+/-1.3 kg.m(-2) were examined. The ghrelin serum levels (165.0+/-58.1 vs. 343.37+/-81.96; p<0.001) and soluble leptin receptor serum levels (7.25+/-3.44 vs. 21.80+/-4.99; p<0.0001) were significantly lower in obese patients. The leptin serum levels (23.45+/-12.90 vs. 6.41+/-2.96; p<0.005) were significantly higher compared to the lean subject group. In both measured groups the levels of serum leptin significantly positively correlated with BMI. We proved a significantly lower serum ghrelin levels in the group of obese patients in comparison with the control group.     

Elevated soluble CD40 ligand in diabetic patients with painless myocardial infarction

Because a useful biomarker for painless myocardial infarction (MI) has yet to be identified, the aim of this study was to identify a biomarker for diabetic patients with painless MI. A case-control design was used to compare inflammatory cytokine levels among 111 patients with diabetes mellitus, including 31 patients with stable coronary heart disease (CHD), 30 patients with painful MI, 20 patients with painless MI, and 30 age- and sex-matched patients without CHD (control group). In addition to baseline parameters, cytokine levels, including plasma high sensitivity C-reactive protein (HsCRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and soluble CD40 ligand (sCD40L) levels, were analyzed using enzyme-linked immunosorbent assays (ELISAs). No differences in baseline characteristics were observed for patients with painless MI as compared to the other patient groups. Significantly higher sCD40L, HsCRP, IL-6, and TNF-α levels were detected in patients with MI, and markedly elevated sCD40L and IL-6 levels were observed in patients with painless MI as compared to those with painful MI. sCD40L may be a useful biomarker for painless MI in diabetic patients, which could reduce misdiagnosis and expedite treatment. Further studies are required to validate the diagnostic utility of this putative biomarker as well as investigate the mechanism by which sCD40L is elevated in these patients.     

A 60-s postconditioning protocol by percutaneous coronary intervention inhibits myocardial apoptosis in patients with acute myocardial infarction

Different postconditioning (Postcon) methods have been demonstrated to protect heart from ischemia/reperfusion injury. The relationship between Postcon by percutaneous coronary intervention (PCI) and apoptosis is not clear. Our objective was to test whether Postcon by PCI in patients with acute myocardial infarction (AMI) reduces myocardial apoptosis. Seventy-five patients were randomly assigned to one of three groups before stenting. The Routine group (n = 26) received no Postcon intervention prior to the onset of reperfusion; Postcon-30s (n = 25) and Postcon-60s groups (n = 24) underwent three cycles of 30- or 60-s balloon deflation and 30- or 60-s inflation. Additionally, 34 normal controls (NC) were enrolled in the study. Plasma concentrations of soluble Fas/APO-1 ([sFas]) and Fas ligand ([sFasL]) were determined at baseline and 7 days after PCI via ELISA. The [sFas] and [sFasL] in AMI patients were significantly elevated at baseline as compared with NC (P < 0.01), and showed an upward trend in the Routine group, a slightly upward trend in Postcon-30s, and a downward trend in Postcon-60s at 7 days. Comparison among the three groups showed significant differences (P < 0.05, 3.8 vs. 4.6 vs. 5.1 ng ml⁻¹). The [sFasL] in Postcon-60s was significantly decreased at 7 days (P < 0.05, 3.9 vs. 3.1 ng ml⁻¹) compared with baseline, but not Postcon-30s and Routine. More importantly, Postcon-60s group had the lowest [sFasL], followed by Postcon-30s, which had a lower value than Routine at 7 days (P < 0.05, 3.1 vs.3.7 vs. 4.2 ng ml⁻¹). Our results suggest that Postcon-60s was visibly better than Postcon-30s, which in turn was better than Routine for inhibition of the effects of myocardial apoptosis and reduction of reperfusion injury in patients with acute myocardial infarction.     

A relation of serum homocysteine and uric acid in Bosnian diabetic patients with acute myocardial infarction

Background: Coronary artery disease as a consequence of atherosclerosis is the most common cause of morbidity and mortality in type 2 Diabetes Mellitus (DM) patients. Homocysteine (HCY), as one of the risk factors, and uric acid (UA) as the most common antioxidant in serum have their roles in the processes of inflammation and atherogenesis, which underlie the pathogenesis of acute myocardial infarction (AMI). The effect of HCY in cardiovascular disease is thought to be manifested primarily through oxidative damage, implying a potential correlation between the HCY level and antioxidant status. Since the data related to the diagnostic significance of both HCY and UA in diabetic patients with AMI are conflicting, and so far not reported in Bosnian patients, this research aimed to examine the association of HCY and UA levels with glomerular filtration rate (eGFR) and explore the pathophysiological significance of these data in Bosnian diabetic patients with AMI. Methods: This prospective research included 52 DM type 2 patients diagnosed with AMI. Blood samples were taken on admission and used for biochemical analysis. Results of the biochemical analyses were statistically analysed. Results: Elevated HCY and UA levels were observed in diabetic patients. Females have higher HCY compared to males. A positive correlation was revealed between HCY and UA and was confirmed with different HCY levels in subgroups with different UA level. A negative correlation was observed between UA and HbA1c, as well as between both HCY and UA with eGFR. Conclusions: These results contribute to the clarification of the biochemical mechanisms characteristic in AMI patients with DM. According to these results, we believe that joint measurement of HCY and UA could enable a better assessment of the prognosis for this group of patients. This kind of assessment, as well as regression analysis, can identify high-risk patients at an earlier stage when appropriate interventions can influence a better outcome in such patients.     

Comparison of high-sensitivity C-reactive protein level between systemic and coronary circulation in patients with acute myocardial infarction

Inflammation plays an important role not only in the initi- ation and progression of atherosclerosis but also in plaque rupture of coronary artery disease （CAD） [ 1 - 3], which leads to acute coronary syndrome （ACS） or even acute myocardial infarction （AMI）. It is well known that C-reactive protein （CRP） is one of the most important inflammation markers and has been proved to be an independent risk factor for CAD [4-7]. High level of CRP predicts poor clinical out- comes in patients with both stable CAD and ACS [6-9]. Compared with CRP, high-sensitivity CRP （hs-CRP） is more sensitive that can be examined in serum. However, the source of CRP or hs-CRP in CAD or ACS has not been definitively explored.     

Impact of tuberculosis on serum leptin levels in patients with HIV infection

AIM: Tuberculosis (TB) and human immunodeficiency virus (HIV) are classical wasting diseases accompanied by immunosuppression. As leptin is involved in the weight regulation and cellular immunity, we investigated the role of leptin levels in the co-infection of HIV and TB (HIV-TB). METHODS: The study group consists of the patients with asymptomatic HIV infection (n = 20), patients with HIV-TB co-infection (n = 20) and healthy control subjects (n = 20). Serum leptin levels and the concentrations of IFN-gamma, TNF-alpha, IL-12 and IL-4 cytokines were measured by ELISA before the start of the treatment. CD4+ T-cell counts were determined in patients with HIV and HIV-TB by flow cytometry. Body mass index (BMI) of the study subjects was calculated. RESULTS: Serum leptin levels and BMI were significantly lower in the patients with HIV-TB than control and HIV subjects. Multivariate regression analysis showed that serum leptin concentration was significantly dependent on BMI and sex but not on age and the disease groups. The leptin levels did not correlate either with CD4+ T-cell counts or with any of the serum cytokines in HIV and HIV-TB patients. CONCLUSION: Thus our finding suggests that the leptin concentrations were strongly associated with BMI and gender but not with the disease state or with the circulating cytokine levels.     

Survival in acute myocardial infarction; factors observed in 318 patients

Factors influencing survival in a group of 318 cases of acute myocardial infarction were analyzed. The mortality rate for the entire series was 41 per cent. Among the men it was 39.5 per cent; among women, 44.4 per cent. The mortality rate increased with the age of the patient. Twenty-six per cent of all deaths occurred within the first 24 hours, 44 per cent within 72 hours, and 71 per cent within the first week following hospital admission. Increased mortality rate was associated with previous history of congestive failure, myocardial infarction, hypertension or cardiomegaly. As to circumstances immediately preceding an infarction, the only ones that seemed to be related to a high mortality rate were hemorrhage and the postoperative state. Not only the presence but the degree of shock, congestive failure, cyanosis and dyspnea adversely influenced chances for survival. Duration, location, radiation and number of attacks of pain did not appear to be associated with extraordinary mortality rates. Anterior was slightly more common than posterior infarctions, and the mortality rate was much higher. Thromboembolic complications and certain disorders of rhythm and of conduction definitely worsen prognosis. Comparison of average mortality data as reported in different studies on acute myocardial infarction is improper and misleading because of the great differences between the kinds of patients included in various series reported upon. A standard method of grading the severity of acute myocardial infarction would help toward sounder comparisons.