Publications (22) View all
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Article: Spontaneous coronary artery dissection: A Western Denmark Heart Registry Study
K.H. Mortensen MD, L. Thuesen MD, I.B. Kristensen MD, E.H. Christiansen MD, K.H. Mortensen, L. Thuesen, I.B. Kristensen, E.H. Christiansen[show abstract] [hide abstract]
ABSTRACT: Background: Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome (ACS) that associates with a high acute-phase mortality rate, whereas long-term outcome is less well described. Objective: To describe the incidence, predictors, and prognosis of SCAD. Design: Retrospective case-identification study from the Western Denmark Heart Registry and the database of the Forensic Institute at Aarhus University from 1999 through 2007. Results: SCAD was documented in 22 of 32,869 (0.7‰) angiograms in the angiographic registry. The SCAD incidence among cases of ACS was 22 of 11,175 (2.0‰). None was seen in the forensic database. The mean age was 48.7 ± 8.9 years (range: 37–71 years). Females constituted 17 of 22 (77%) patients and all had undergone one or more pregnancies; two cases occurred in the postpartum period. The left descending artery (LAD) was the predominant site of entry. The age distribution, prevalence of the cardiovascular risk factors, presence of coronary atherosclerosis, and entry of the dissection were comparable among genders. Treatment was percutaneous coronary intervention in 13 of 22 (59%), coronary artery bypass operation in 2 of 22 (9%), and medical treatment in 7 of 22 (32%) patients. The mean follow-up period was 3.6 ± 2.9 years. One patient suffered from recurrent SCAD; another patient died suddenly. The MACE- (cardiac death, nonfatal myocardial infarction, and new revascularization) free survival was 81% after 24 months. Conclusion: SCAD is a rare disease that mainly affects younger women. Compared with earlier reports, the prognosis seems to be improved by early diagnosis and interventional treatment. © 2009 Wiley-Liss, Inc.Catheterization and Cardiovascular Interventions 10/2009; 74(5):710 - 717. · 2.29 Impact Factor -
Article: Spontaneous coronary artery dissection: a Western Denmark Heart Registry study.
[show abstract] [hide abstract]
ABSTRACT: Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome (ACS) that associates with a high acute-phase mortality rate, whereas long-term outcome is less well described. To describe the incidence, predictors, and prognosis of SCAD. Retrospective case-identification study from the Western Denmark Heart Registry and the database of the Forensic Institute at Aarhus University from 1999 through 2007. SCAD was documented in 22 of 32,869 (0.7 per thousand) angiograms in the angiographic registry. The SCAD incidence among cases of ACS was 22 of 11,175 (2.0 per thousand). None was seen in the forensic database. The mean age was 48.7 +/- 8.9 years (range: 37-71 years). Females constituted 17 of 22 (77%) patients and all had undergone one or more pregnancies; two cases occurred in the postpartum period. The left descending artery (LAD) was the predominant site of entry. The age distribution, prevalence of the cardiovascular risk factors, presence of coronary atherosclerosis, and entry of the dissection were comparable among genders. Treatment was percutaneous coronary intervention in 13 of 22 (59%), coronary artery bypass operation in 2 of 22 (9%), and medical treatment in 7 of 22 (32%) patients. The mean follow-up period was 3.6 +/- 2.9 years. One patient suffered from recurrent SCAD; another patient died suddenly. The MACE- (cardiac death, nonfatal myocardial infarction, and new revascularization) free survival was 81% after 24 months. SCAD is a rare disease that mainly affects younger women. Compared with earlier reports, the prognosis seems to be improved by early diagnosis and interventional treatment.Catheterization and Cardiovascular Interventions 06/2009; 74(5):710-7. · 2.29 Impact Factor -
SourceAvailable from: Claus Højbjerg Gravholt
Article: Carotid intima-media thickness is increased in Turner syndrome: multifactorial pathogenesis depending on age, blood pressure, cholesterol and oestrogen treatment.
Kristian Havmand Mortensen, Niels Holmark Andersen, Britta Eilersen Hjerrild, Arne Hørlyck, Kirstine Stochholm, Claus Højbjerg Gravholt[show abstract] [hide abstract]
ABSTRACT: Objective: Carotid intima-media thickness (IMT) may potentially supplement cardiovascular risk assessment in Turner syndrome (TS), where cardiovascular risk is high and appropriate risk stratification difficult. Knowledge of intima-media thickness in TS is scarce, and this study aimed to enhance insight into the cardiovascular risk marker. Design, Patients and Measurements: IMT was cross-sectionally assessed by ultrasonography of the common carotid artery (cIMT) and carotid bulb (bIMT) in TS (n=69, age 40 ± 10 years) and age-matched, healthy female controls (n=67). Additional prospective IMT assessment was performed in TS over 2.4 ± 0.3 years. Metabolic biomarkers and 24-hour ambulatory blood pressure were also assessed. Results: cIMT and bIMT (body surface area indexed) were increased in TS (P<0.05) with 17-18% having IMTs that exceeded the 95(th) percentile of the controls (P<0.05). Blood pressure, heart rate, HbA1c and high-density lipoprotein cholesterol were increased in TS, where 43% received antihypertensive treatment. cIMT decreased during follow-up, coinciding with intensified cardiovascular risk prophylaxis whereas bIMT was unchanged. In multiple regression analyses (R=0.52-0.69, P<0.05) baseline IMT in TS increased with age, blood pressure and cholesterol as well as in the presence of diabetes whilst IMT was inversely associated with duration of oestrogen replacement. In an analogue analysis, the prospective changes in cIMT (R=0.37, P<0.05) were beneficially influenced by antihypertensive treatment and oestrogen therapy and adversely by the presence of diabetes. Conclusion: Carotid IMT was abnormal in TS and negatively influenced by age, metabolic biomarkers, blood pressure and short duration of oestrogen treatment. Attention to common cardiovascular and endocrine risk markers over more than two years appeared to influence IMT beneficially. © 2012 Blackwell Publishing Ltd.Clinical Endocrinology 01/2012; · 3.17 Impact Factor -
SourceAvailable from: Claus Højbjerg Gravholt
Article: Cardiovascular phenotype in turner syndrome--integrating cardiology, genetics, and endocrinology.
Kristian H Mortensen, Niels H Andersen, Claus H Gravholt[show abstract] [hide abstract]
ABSTRACT: Cardiovascular disease is emerging as a cardinal trait of Turner syndrome, being responsible for half of the 3-fold excess mortality. Turner syndrome has been proposed as an independent risk marker for cardiovascular disease that manifests as congenital heart disease, aortic dilation and dissection, valvular heart disease, hypertension, thromboembolism, myocardial infarction, and stroke. Risk stratification is unfortunately not straightforward because risk markers derived from the general population inadequately identify the subset of females with Turner syndrome who will suffer events. A high prevalence of endocrine disorders adds to the complexity, exacerbating cardiovascular prognosis. Mounting knowledge about the prevalence and interplay of cardiovascular and endocrine disease in Turner syndrome is paralleled by improved understanding of the genetics of the X-chromosome in both normal health and disease. At present in Turner syndrome, this is most advanced for the SHOX gene, which partly explains the growth deficit. This review provides an up-to-date condensation of current state-of-the-art knowledge in Turner syndrome, the main focus being cardiovascular morbidity and mortality. The aim is to provide insight into pathogenesis of Turner syndrome with perspectives to advances in the understanding of genetics of the X-chromosome. The review also incorporates important endocrine features, in order to comprehensively explain the cardiovascular phenotype and to highlight how raised attention to endocrinology and genetics is important in the identification and modification of cardiovascular risk.Endocrine reviews 06/2012; 33(5):677-714. · 19.76 Impact Factor -
SourceAvailable from: Claus Højbjerg Gravholt
Article: Increased prevalence of autoimmunity in Turner syndrome--influence of age.
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ABSTRACT: Individuals with Turner syndrome (TS) are prone to develop autoimmune conditions such as coeliac disease (CD), thyroiditis and type 1 diabetes (T1DM). The objective of the present study was to examine TS of various karyotypes for autoantibodies and corresponding diseases. This was investigated in a prospective cross-sectional study of Danish TS patients (n = 107, median age 36.7 years, range: 6-60 years). A medical history was recorded and a blood sample was analysed for autoantibodies against gliadin, transglutaminase, adrenal cortex, intrinsic factor, anti-thyroid peroxidase (anti-TPO) and glutamic-acid-decarboxylase 65 (GAD-65). Autoantibodies were present in 58% (n = 61) of all patients, whereof 18% (11) had autoantibodies targeting more than one organ. Patients with autoantibodies were significantly older than those without (P = 0.001). Anti-TPO was present in 45% (48) of patients, of whom 33% (16) were hypothyroid. Overall, 18% (19) presented with CD autoantibodies, of whom 26% (five) had CD. Anti-TPO and CD autoantibodies co-existed in 9% (10). Immunoglobulin A deficiency was found in 3% (three) of patients, who all had CD autoantibodies without disease. Among four patients with anti-GAD-65 none had T1DM, but two were classified as having T2DM. One patient had adrenocortical autoantibodies but not adrenal failure. Autoantibodies against intrinsic factor were absent. Anti-GAD-65 was increased in isochromosomal karyotypes (3/23 versus 1/84, P = 0.008) with no other association found between autoantibodies and karyotype. In conclusion, TS girls and women face a high prevalence of autoimmunity and associated disease with a preponderance towards hypothyroidism and CD. Thus, health care providers dealing with this patient group should be observant and test liberally for these conditions even before clinical symptoms emerge.Clinical & Experimental Immunology 03/2009; 156(2):205-10. · 3.36 Impact Factor