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J C Kaski

Publications and source records attributed to J C Kaski.

At least 19 recordsLinked to original sources
PubMed2006

Prediction of infarction-related artery occlusion and multivessel disease in postinfarction angina.

CONDENSED ABSTRACT: To investigate the predictive value of clinical data for infarction-related artery (IRA) occlusion and multivessel coronary disease in postinfarction angina (PIA), we studied 181 consecutive patients presenting PIA following a first uncomplicated ST elevation AMI. Multivariate analysis showed ECG changes during PIA and the absence of thrombolytic therapy as independent predictors of IRA occlusion. Independent clinical predictors of multivessel coronary disease were age, previous history of angina and the number of cardiovascular risk factors. We conclude that reversible ECG changes during PIA correlated to IRA occlusion but failed to predict a multivessel coronary disease. AIM: To identify clinical variables predictive of infarction-related artery (IRA) occlusion and multivessel coronary disease in patients with postinfarction angina pectoris (PIA) after a first uncomplicated acute myocardial infarction (AMI). METHODS: We studied 181 consecutive patients with PIA following a first uncomplicated AMI. Clinical variables included cardiovascular risk factors, clinical history of angina before the event of inclusion, use of thrombolytic therapy in the previous AMI, ST-T changes during PIA, time to onset, number of episodes and delay to angiography after PIA. Angiographic variables were IRA TIMI flow, number of diseased vessels and ventricular function. RESULTS: The IRA was occluded in 67 patients with PIA (37.0%). Reversible ECG changes during PIA were detected in 121 patients (67.0%): 79 cases (43.6%) with ST/T elevation and 42 cases (23.2%) with ST/T depression. Multivariate logistic regression analysis showed ECG changes during PIA (OR 3.12 CI 95% 1.48-6.54, p<0.01) and the absence of thrombolytic therapy (OR 2.21 95% CI 1.11-4.43, p<0.05) as independent predictors of IRA occlusion. We found multivessel coronary disease in 89 patients (49.2%) without any correlation to ECG changes during PIA. Independent clinical predictors of multivessel coronary disease were age (OR 1.03 95% CI 1.01-1.06, p<0.05), previous history of angina (OR 2.37 95% CI 1.06-5.28, p<0.05) and the number of cardiovascular risk factors (OR 1.37 95% CI 0.97-1.92, p=0.07). CONCLUSIONS: ECG changes during PIA was correlated to IRA occlusion in spite of previous thrombolytic therapy but failed to predict a multivessel coronary disease in our patients.

Adult↗
PubMed2006

Cardiac syndrome X in women: the role of oestrogen deficiency.

Cardiac syndrome X (CSX), defined as typical exertional chest pain, a positive response to stress testing, and normal coronary arteriograms, encompasses different pathogenic subgroups. Both cardiac and non-cardiac mechanisms have been suggested to play a pathogenic role, and it has been shown that the syndrome is associated with myocardial ischaemia in at least a proportion of patients. Radionuclide myocardial perfusion defects, coronary sinus oxygen saturation abnormalities and pH changes, myocardial lactate production and stress-induced alterations of cardiac high energy phosphate have been reported in CSX patients, suggesting an ischaemic origin for their symptoms. Microvascular abnormalities often caused by endothelial dysfunction appear to be responsible for myocardial ischaemia in these patients. CSX is more prevalent in women than in men, and the majority of women with CSX are peri- or post-menopausal. Thus oestrogen deficiency has been suggested to have a pathogenic role in CSX. Additional factors such as abnormal pain perception may also contribute to the genesis of chest pain in patients with angina and normal coronary angiograms. The management of this syndrome is difficult because of the heterogeneity of pathogenic mechanisms and uncertainties as to its origin. This article discusses the problem of CSX in women, the potential pathogenic role of oestrogen deficiency, and practical clinical management.

Endothelium, Vascular↗
PubMed2005

Detection of Chlamydia pneumoniae in atherosclerotic tissue: a comparative study of PCR and immunocytochemistry.

The reported prevalence of Chlamydia pneumoniae in atherosclerotic tissue appears to depend on the detection system used. This introduces problems in determining the role of C. pneumoniae in atherosclerosis. This study analyses the sensitivity and performance of molecular diagnostic methods for the detection of C. pneumoniae and polymerase chain reaction (PCR) inhibitors in atheromatous tissue. Atherosclerotic tissue taken from 30 coronary endarterectomies, nine coronary arteries from explanted hearts, 16 carotid and two femoral endarterectomies are studied. Nested PCR (nPCR) assays targeting the PstI restriction fragment, the OmpA gene and the CRP operon of the chlamydial genome and immunocytochemistry (ICC) are used. Internal controls (IC) are constructed to co-amplify with the specific amplicons and identify the presence of inhibitor. The OmpA, PstI and CRP operon PCR assays had similar analytical sensitivities. However, the OmpA PCR was most affected by PCR inhibitors. Despite this, eight samples (14%) tested positive in the OmpA nPCR and no positives were found using the PstI or CRP operon nPCRs. Primary isolates of C. pneumoniae obtained from 12 patients with acute respiratory infection were positive in all three assays. Of the 48 specimens available for ICC, 33 (69%) were positive for chlamydial antigens. These included samples found positive by PCR. Dilution of samples to eliminate PCR inhibitors may have contributed to the discordant ICC and PCR results. The OmpA PCR, when used with an IC to identify samples with PCR inhibitors, is a reliable tool. However, the sensitivity of the ICC methods justifies their continued use.

Adult↗
PubMed2005

Matrix metalloproteinase-9 expression is associated with the presence of Chlamydia pneumoniae in human coronary atherosclerotic plaques.

OBJECTIVE: To investigate the association between Chlamydia pneumoniae and matrix metalloproteinase-9 (MMP-9) in atherosclerotic plaques. DESIGN: 31 coronary atherosclerotic plaque specimens were studied by immunohistochemistry, polymerase chain reaction (PCR), and reverse transcription PCR for the presence of C pneumoniae antigen and genomic DNA, and of MMP-9 protein and transcripts. RESULTS: Immunohistochemical analysis identified a strong association between the presence of C pneumoniae antigen and production of MMP-9 in coronary atherosclerotic plaques (p = 0.001). Furthermore, analysis of the intralesional amount of C pneumoniae and MMP-9 indicated an increased number of cells positive for MMP-9 in arterial sections that had increased C pneumoniae positivity (p < 0.05). CONCLUSIONS: This study provides evidence of an association between expression of MMP-9 and the intravascular presence of C pneumoniae and may suggest a potential pathological mechanism whereby C pneumoniae may contribute to the progression of coronary atherosclerosis.

Adult↗
PubMed2005

Inflammatory biomarkers of coronary atheromatous plaque vulnerability.

In the last decade, compelling evidence has evolved at both the basic science and clinical level for the implication of inflammation in the pathogenesis of atherosclerosis and its complications. The composition of the atherosclerotic plaque, rather than the degree of stenosis, is now recognized as a pivotal feature in determining plaque vulnerability and hence the risk of acute coronary ischaemic events. Current evidence supports a key role for inflammation in all phases of the atherosclerotic process, from plaque formation through to progression and, ultimately, the thrombotic complications of atherosclerosis. The growing appreciation of the role of inflammation in atherogenesis has focused attention on whether circulating levels of inflammatory biomarkers may help to identify those at risk of future cardiovascular events. In addition, the protective effects of a variety of interventions, such as statins, aspirin, and fibrates, are often associated with the evidence of reduced inflammation, further strengthening the notion that inflammation and the acute complications of atherosclerosis are causally related. The present review describes the pathophysiology of atheromatous plaque vulnerability and discusses the clinical use of inflammatory biomarkers for prognostic stratification of patients with acute coronary syndromes.

Biomarkers↗
PubMed2004

Role of "Ischemia modified albumin", a new biochemical marker of myocardial ischaemia, in the early diagnosis of acute coronary syndromes.

BACKGROUND: Diagnosis of cardiac ischaemia in patients attending emergency departments (ED) with symptoms of acute coronary syndromes is often difficult. Cardiac troponin (cTn) is sensitive and specific for the detection of myocardial damage but may not rise during reversible myocardial ischaemia. Ischemia Modified Albumin (IMA) has recently been shown to be a sensitive and early biochemical marker of ischaemia. METHODS AND RESULTS: This study evaluated IMA in conjunction with ECG and cTn in 208 patients presenting to the ED within three hours of acute chest pain. At presentation, a 12-lead ECG was recorded and blood taken for IMA and cardiac troponin T (cTnT). Patients underwent standardised triage, diagnostic procedures, and treatment. Results of IMA, ECG, and cTnT, alone and in combination, were correlated with final diagnoses of non-ischaemic chest pain, unstable angina, ST segment elevation, and non-ST segment elevation myocardial infarction. In the whole patient group, sensitivity of IMA at presentation for an ischaemic origin of chest pain was 82%, compared with 45% of ECG and 20% of cTnT. IMA used together with cTnT or ECG, had a sensitivity of 90% and 92%, respectively. All three tests combined identified 95% of patients whose chest pain was attributable to ischaemic heart disease. In patients with unstable angina, sensitivity of IMA used alone was equivalent to that of IMA and ECG combined. CONCLUSIONS: IMA is highly sensitive for the diagnosis of myocardial ischaemia in patients presenting with symptoms of acute chest pain.

Adult↗
PubMed2004

CD14 and toll-like receptor 4: a link between infection and acute coronary events?

The CD14 receptor is a pattern recognition molecule in the innate immune response against microorganisms and other exogenous and endogenous stress factors. The most important CD14 signalling co-receptor is toll-like receptor 4 (TLR4), which activates, among others, the nuclear factor kappaB (NF-kappaB) inflammatory pathway. Besides its role in innate immunity and host defence, the proinflammatory cytokines expressed upon TLR4/NF-kappaB pathway activation exert proatherogenic effects. The CD14 C(-260)T promoter and TLR4 Asp299Gly functional polymorphisms have been recently implicated in the development of cardiovascular events, suggesting that the genetically determined inflammatory response against pathogens or their antigens may have a major role in atherogenesis and subsequent acute events. Is the association of these polymorphisms with cardiovascular disease more evidence for the implication of infection, especially by Gram negative bacteria, in the development of acute coronary events? This article reviews the molecular basis, biological functions, and clinical implications of the CD14/TLR4 polymorphisms in the development of cardiovascular events.

Cell Communication↗
PubMed2004

Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes.

OBJECTIVE: To assess the relation between markers of inflammation and the presence of multiple vulnerable plaques in patients with non-ST segment elevation acute coronary syndromes. DESIGN: Prospective cohort study of 55 patients with non-ST segment elevation acute coronary syndromes and angiographically documented coronary disease. Blood samples were obtained at study entry for the assessment of high sensitivity C reactive protein (CRP), neopterin, and neutrophil count. Coronary stenoses were assessed by quantitative computerised angiography and classified as "complex" (irregular borders, ulceration, or filling defects) or "smooth" (absence of complex features). Extent of disease was also assessed by a validated angiographic score. RESULTS: Neutrophil count (r = 0.36, p = 0.007), CRP concentration (r = 0.33, p = 0.02), and neopterin concentration (r = 0.45, p < 0.001) correlated with the number of complex stenoses. Patients with multiple (three or more) complex stenoses, but not patients with multiple smooth lesions, had a higher neutrophil count (5.9 (1.4) x 10(9)/l v 4.8 (1.4) x 10(9)/l, p = 0.02), CRP concentration (log transformed) (1.08 (0.63) v 0.6 (0.6), p = 0.03), and neopterin concentration (log transformed) (0.94 (0.18) v 0.79 (0.15), p = 0.002). Multiple regression analysis showed that neopterin concentration (B = 4.8, 95% confidence interval (CI) 1.9 to 7.7, p = 0.002) and extent of coronary artery disease (B = 0.6, 95% CI 0.03 to 1.2, p = 0.04) were independently associated with the number of complex stenoses. CONCLUSIONS: Acute inflammatory markers such as high neutrophil count, CRP concentration, and neopterin concentration correlate with the presence of multiple angiographically complex coronary stenoses. Neopterin concentration was a stronger predictor of multiple complex plaques than were neutrophil count and CRP concentration. These findings suggest that a relation exists between inflammation and pancoronary plaque vulnerability.

Angina, Unstable↗
PubMed2001

Serum levels of the antiinflammatory cytokine interleukin-10 are decreased in patients with unstable angina.

BACKGROUND: Proinflammatory cytokines play a role in acute coronary events. However, the potential role of antiinflammatory cytokines in the modulation of the atherosclerotic process remains unknown. Interleukin (IL)-10, which is expressed in human atherosclerotic plaques, has potent deactivating properties in macrophages and T cells. The aim of this study was to assess whether serum concentrations of IL-10 differed between patients with unstable and stable angina pectoris. METHODS AND RESULTS: A total of 95 patients with angina pectoris and angiographically documented coronary artery disease were studied. Of these, 50 patients had chronic stable angina (with stable symptoms over 3 months), and 45 patients had Braunwald class IIIB unstable angina with ST-segment changes. Serum IL-10 and IL-6 concentrations were measured on admission using commercially available immunoassays. Serum IL-10 concentrations were lower in unstable angina patients compared with those who had chronic stable angina (28.4 versus 14.0 pg/mL; 95% CI, 9.8 to 19.0; P<0.0001), even after adjustment for variables that were significantly different on univariate analysis. IL-6 concentrations were higher in the unstable angina group (20.9 versus 11.4 pg/mL; 95% CI, 1.0 to 12.6; P=0.04). CONCLUSIONS: Patients with unstable angina had significantly lower serum IL-10 concentrations than did patients with chronic stable angina. This important finding is in keeping with previous data from animal model studies that suggest that IL-10 has a protective role in atherosclerosis.

Acute Disease↗
PubMed2001

Vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 serum level in patients with chest pain and normal coronary arteries (syndrome X).

BACKGROUND: Plasma levels of soluble vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) mediators of leukocyte adhesion to vascular endothelium may implicate in the pathogenesis of the syndrome of chest pain with normal coronary arteries. HYPOTHESIS: We attempted to determine whether markers of endothelial activation are raised in patients with chest pain and normal coronary arteries. METHODS: We measured plasma VCAM-1, ICAM-1 (ng/ ml) in 36 patients (34 men, 2 women, aged 62 +/- 9 years) with stable angina, coronary artery disease (CAD), and a positive response to exercise test; in 21 patients (6 men, 15 women, aged 56 +/- 9 years) with chest pain and normal coronary arteriograms (syndrome X); and in 11 healthy control subjects (8 men, 3 women, aged 49 +/- 14 years). RESULTS: Plasma ICAM-1 levels were significantly higher both in patients with CAD (mean +/- standard error of the mean) (328 +/- 26, p < 0.05), and in syndrome X (362 +/- 22, p < 0.01) than in controls (225 +/- 29). VCAM-1 levels were also higher in syndrome X (656 +/- 42 ng/ml) and in patients with CAD (626 +/- 42 ng/ml) than in controls (551 +/- 60, p = 0.09). CONCLUSIONS: ICAM-1 and VCAM-1 levels are increased both in patients with CAD and with syndrome X compared with control individuals. These findings may suggest the presence of chronic inflammation with involvement of the endothelium in patients with anginal chest pain and normal coronary angiograms.

Adult↗
PubMed2001

Increased QT dispersion in patients with Prinzmetal's variant angina and cardiac arrest.

OBJECTIVES: We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. BACKGROUND: Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic angina patients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. METHODS: We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses < or =40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum-QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. RESULTS: Mean (+/-S.D.) QT dispersion of study patients was 62.3+/-19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4+/-17.3 ms) was significantly higher compared to patients with no such events (56.3+/-16.9 ms), (95% CI 7.5-38.8, P=0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. CONCLUSION: QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.

Adult↗