γ‐Glutamyltransferase and Risk of Sudden Cardiac Death in Middle‐Aged Finnish Men: A New Prospective Cohort Study

Kunutsor, Setor K; Khan, Hassan; Laukkanen, Jari A.

doi:10.1161/jaha.115.002858

Cited by 23 publications

(27 citation statements)

References 48 publications

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“…In the KIHD study, the HR for an association of GGT with the risk of ventricular arrhythmias was 1.37 (1.04-1.80) (66). A recent publication from the KIHD study showed that serum GGT was log-linearly associated with the risk of sudden cardiac death with a HR =1.30 (10-1.54) per each SD higher log GGT (79). The association of GGT with sudden cardiac death remained significant after adjustment for known risk factors, alcohol consumption, resting heart rate, lipids and C-reactive protein [HR =1.26 (1.05-1.50)].…”

Section: Ggt Cardiac Arrhythmias and Sudden Cardiac Deathmentioning

confidence: 99%

Gamma-glutamyl transferase and cardiovascular disease

Ndrepepa¹,

Kastrati²

2016

Ann. Transl. Med.

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Gamma-glutamyl transferase (GGT) is an enzyme located on the external surface of cellular membranes. GGT contributes in maintaining the physiological concentrations of cytoplasmic glutathione and cellular defense against oxidative stress via cleavage of extracellular glutathione and increased availability of amino acids for its intracellular synthesis. Increased GGT activity is a marker of antioxidant inadequacy and increased oxidative stress. Ample evidence suggests that elevated GGT activity is associated with increased risk of cardiovascular disease (CVD) such as coronary heart disease (CHD), stroke, arterial hypertension, heart failure, cardiac arrhythmias and all-cause and CVD-related mortality. The evidence is weaker for an association between elevated GGT activity and acute ischemic events and myocardial infarction. The risk for CVD or CVD-related mortality mediated by GGT may be explained by the close correlation of GGT with conventional CVD risk factors and various comorbidities, particularly non-alcoholic fatty liver disease, alcohol consumption, oxidative stress, metabolic syndrome, insulin resistance and systemic inflammation. The finding of GGT activity in atherosclerotic plaques and correlation of intra-plaque GGT activity with histological indexes of plaque instability may suggest a participation of GGT in the pathophysiology of CVD, particularly atherosclerosis. However, whether GGT has a direct role in the pathophysiology of CVD or it is an epiphenomenon of coexisting CVD risk factors or comorbidities remains unknown and Hill's criteria of causality relationship between GGT and CVD are not fulfilled. The exploration whether GGT provides prognostic information on top of the information provided by known cardiovascular risk factors regarding the CVD or CVD-related outcome and exploration of molecular mechanisms of GGT involvement in the pathophysiology of CVD and eventual use of interventions to reduce circulating GGT activity remain a duty of future studies.

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Section: Ggt Cardiac Arrhythmias and Sudden Cardiac Deathmentioning

confidence: 99%

Gamma-glutamyl transferase and cardiovascular disease

Ndrepepa¹,

Kastrati²

2016

Ann. Transl. Med.

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“…Detailed description of blood sample collection, physical measurements, assessment of lifestyle characteristics, and assays for lipids, lipoproteins and biochemical factors have been provided in previous reports. [15,16] Serum levels of triglycerides were assessed enzymatically (Boehringer Mannheim, Mannheim, Germany). Fasting plasma glucose was measured by the glucose dehydrogenase method (Merck, Darmstadt, Germany) after protein precipitation by trichloroacetic acid.…”

Section: Assessment Of Covariatesmentioning

confidence: 99%

Associations of cardiovascular and all-cause mortality events with oxygen uptake at ventilatory threshold

Kunutsor

Kurl

Khan

et al. 2017

International Journal of Cardiology

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms Abbreviations BMI = body mass index CHD = coronary heart disease CRF = cardiorespiratory fitness CVD = cardiovascular disease HDL-C = high-density lipoprotein cholesterol HR = hazard ratio IDI = integrated-discrimination-improvement KIHD = Kuopio Ischaemic Heart Disease NRI = net reclassification improvement SCD = sudden cardiac death SD = standard deviation SBP = systolic blood pressure VT = ventilatory threshold VO2 = oxygen uptake ABSTRACTBackground: Oxygen uptake (VO2) at ventilatory threshold (VT), is a cardiopulmonary exercise testing parameter which may be a proxy for peak VO2. We aimed to assess the associations of VO2 at VT with sudden cardiac death (SCD), fatal coronary heart disease (CHD) and cardiovascular disease (CVD), and all-cause mortality.Methods and Results: VO2 at VT was assessed during a submaximal exercise test using respiratory gas analyzers in the Kuopio Ischemic Heart Disease cohort of 1,639 middle-aged men. Hazard ratios (HRs) (95% CIs) were assessed. During a median follow-up of 25.6 years, 121 SCDs, 202 fatal CHDs, 312 fatal CVDs, and 703 all-cause mortality events occurred. VO2 at VT was correlated with peak VO2 (r = 0.90) and linearly associated with each outcome. Comparing extreme quartiles of VO2 at VT, the HRs (95% CIs) for SCD, fatal CHD, fatal CVD, and all-cause mortality on adjustment for established risk factors Conclusions: There are linear and inverse associations of VO2 at VT with fatal cardiovascular and allcause mortality events, which are dependent on peak VO2. Inclusion of VO2 at VT in the standard established risk factors panel significantly improves the prediction and classification of long-term CVD mortality risk.

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“…[18,19] The cholesterol content of lipoprotein fractions were measured from fresh samples after combined ultracentrifugation and precipitation, and serum triglycerides were assessed enzymatically (Boehringer Mannheim, Mannheim, Germany). [20] Measurement of Lp(a) concentrations were made from frozen plasma samples stored at -20° C for 2-6 years, using a radioimmunoassay (Mercodia Apo(a) RIA, Mercodia AB, Uppsala, Sweden).…”

Section: Measurement Of Risk Factorsmentioning

confidence: 99%

“…The ECG criterion for left ventricular hypertrophy (LVH) was based on either the Sokolow-Lyon or Romhilt-Estes point score as described previously. [18,19] …”

Section: Measurement Of Risk Factorsmentioning

confidence: 99%

Lipoprotein(a) and risk of sudden cardiac death in middle-aged Finnish men: A new prospective cohort study

Kunutsor

Khan

Nyyssönen

et al. 2016

International Journal of Cardiology

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Link to publication record in Explore Bristol Research PDF-document This is the author accepted manuscript (AAM). The final published version (version of record) is available online via Elsevier at http://www.sciencedirect.com/science/article/pii/S0167527316310774. Please refer to any applicable terms of use of the publisher. University of Bristol -Explore Bristol Research General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Finland, supported the Kuopio Ischemic Heart Disease Study. These sources had no role in design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript. 2 Conflicts of interest:The authors report no relationships that could be construed as a conflict of interest.Keywords: Lipoprotein(a); risk factor; risk prediction; sudden cardiac death Lipoprotein(a) levels were log-linearly associated with risk of SCD. In analyses adjusted for established risk factors, the HR (95% CI) for SCD per 1 standard deviation (3.56-fold) higher baseline loge Lp(a) was 1.24 (1.05-1.47; P = 0.013). This remained consistent on further adjustment for alcohol consumption, resting heart rate, lipids, and C-reactive protein 1.23 (1.04-1.46; P = 0.018). HRs remained unchanged after accounting for incident coronary events and did not vary importantly in several relevant clinical subgroups. Adding Lp(a) to a SCD risk prediction model did not significantly improve risk discrimination beyond established risk factors, but improved the continuous net reclassification 30.2% (1.1 to 59.2%, P=0.042).Conclusions: Available evidence shows a continuous and independent association between Lp(a) levels and risk of SCD. Further research is needed to replicate these findings.

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γ‐Glutamyltransferase and Risk of Sudden Cardiac Death in Middle‐Aged Finnish Men: A New Prospective Cohort Study

Cited by 23 publications

References 48 publications

Gamma-glutamyl transferase and cardiovascular disease

Gamma-glutamyl transferase and cardiovascular disease

Associations of cardiovascular and all-cause mortality events with oxygen uptake at ventilatory threshold

Lipoprotein(a) and risk of sudden cardiac death in middle-aged Finnish men: A new prospective cohort study

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