Publications by authors named "Havndrup O"

Background: Imaging-guided percutaneous coronary intervention (PCI) is associated with better clinical outcomes than angiography-guided PCI. Whether routine optical coherence tomography (OCT) guidance in PCI of lesions involving coronary-artery branch points (bifurcations) improves clinical outcomes as compared with angiographic guidance is uncertain.

Methods: We conducted a multicenter, randomized, open-label trial at 38 centers in Europe.

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  • Chronic total occlusions (CTO) are common in patients with coronary artery disease, and while percutaneous coronary intervention (PCI) is a viable treatment, more randomized studies are needed to compare its effectiveness against optimal medical therapy (OMT) alone.
  • This trial assesses the impact of CTO-PCI on patients with myocardial ischemia and determines effects on quality of life and major adverse cardiac and cerebral events (MACCE) through a randomized approach following an initial period of OMT.
  • The results will provide insights that could influence future guidelines on the treatment of chronic total occlusions, depending on whether CTO-PCI shows significant benefits.
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  • Approximately half of young patients with atrioventricular block (AVB) don’t have a known cause; this study looked into potential genetic factors in these cases.
  • Researchers analyzed data from a Danish registry to find patients under 50 who received a pacemaker for AVB, and invited 226 out of 471 identified patients for genetic screening.
  • They found genetic variants linked to AVB in 12 patients (5%), with most variants related to family history of AVB or sudden cardiac death, indicating the importance of genetic testing for diagnosis and risk assessment.
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Background: In patients suspected of acute coronary syndrome, but where the coronary angiography (CAG) has shown unobstructed coronary arteries differential diagnoses include spontaneous coronary artery dissection and takotsubo cardiomyopathy. This case report presents a patient with spontaneous coronary artery dissection but diagnostic signs suspicious of takotsubo cardiomyopathy. Which leads to a consideration of the co-existence of the diseases.

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  • Mitochondrial DNA haplogroup H is linked to a higher risk of hypertrophic cardiomyopathy (HCM), though specific SNPs associated with this risk have not been identified.
  • A study compared the distribution of H haplogroup subtypes in 55 HCM patients with two control groups from Denmark and found a higher proportion of the H3 subtype in the HCM group.
  • The distinct proportions of H subhaplogroups suggest a difference between HCM cases and controls, although the significance of these differences remains unclear without further functional studies.
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Interventional cardiology in Denmark has been carried out since the mid 1980s. Interventional cardiology is only performed at a few high-volume centres. Healthcare coverage is universal and is essentially free of charge.

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Objective: There is a lack of disease-modifying treatments in hypertrophic cardiomyopathy (HCM). The aim of this randomised, placebo-controlled study was to assess if losartan could improve or ameliorate deterioration of cardiac function and exercise capacity.

Methods: Echocardiography, exercise test and MRI or CT were performed at baseline and after 12 months in 133 patients (52±13 years, 35% female) randomly allocated to losartan (100 mg/day) or placebo.

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Identification of the first echocardiographic manifestations of hypertrophic cardiomyopathy may be important for clinical management and our understanding of the pathogenesis. We studied the development of pre-diagnostic echocardiographic changes in young relatives to HCM patients during long-term years follow-up. HCM-relatives not fulfilling the diagnostic criteria for HCM and age of <18 years were included in this study.

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Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disease primarily caused by mutations in genes coding for sarcomeric proteins. A molecular-genetic etiology can be established in ~60% of cases. Evolutionarily conserved mitochondrial DNA (mtDNA) haplogroups are susceptibility factors for HCM.

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Background: No medical treatment has been reliably shown to halt or reverse disease progression in hypertrophic cardiomyopathy, but the results of several pilot studies have suggested beneficial effects of angiotensin II receptor blockers on left ventricular hypertrophy and fibrosis, which are predictive of an adverse outcome. We aimed to assess the effect of the angiotensin II receptor blocker losartan on left ventricular hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy.

Methods: In this single-centre, randomised, double-blind, placebo-controlled trial, adult patients (aged 18 years and older) with obstructive or non-obstructive hypertrophic cardiomyopathy were randomly assigned via computer-based system to losartan (100 mg per day) or placebo for 12 months.

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Background: The widespread use of coronary stents has exposed a growing population to the risk of stent thrombosis, but the importance in terms of risk of ST-segment elevation myocardial infarctions (STEMIs) remains unclear.

Methods: We studied five years follow-up data for 2,098 all-comer patients treated with coronary stents in the randomized SORT OUT II trial (mean age 63.6 yrs.

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Several cardiac diseases are autosomal dominantly inherited. This includes cardiomyopathies, primary arrhythmias (channelopathies), dyslipidaemias, premature ischaemic heart diseases and diseases of the thoracic aorta. Sudden cardiac death in the young is also often due to one of the inherited cardiac diseases.

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Aims: Lesion of the atrioventricular conduction system is a well known adverse effect of alcohol septal ablation (ASA) in patients with obstructive hypertrophic cardiomyopathy (HCM). We assessed the atrioventricular conduction at long-term follow-up after ASA.

Methods: In patients with a pacemaker implanted for high-grade atrioventricular block after ASA, the atrioventricular conduction was assessed prospectively by ECGs and 48-h Holter recordings.

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Mitochondrial dysfunction is a characteristic of heart failure. Mutations in mitochondrial DNA, particularly in MT-CYB coding for cytochrome B in complex III (CIII), have been associated with isolated hypertrophic cardiomyopathy (HCM). We hypothesized that MT-CYB mutations might play an important causal or modifying role in HCM.

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Hypertrophic cardiomyopathy (HCM) is a genetic disorder caused by mutations in genes coding for proteins involved in sarcomere function. The disease is associated with mitochondrial dysfunction. Evolutionarily developed variation in mitochondrial DNA (mtDNA), defining mtDNA haplogroups and haplogroup clusters, is associated with functional differences in mitochondrial function and susceptibility to various diseases, including ischemic cardiomyopathy.

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Background: The penetrance of hypertrophic cardiomyopathy (HCM) during childhood and adolescence has been only sparsely described. We studied the penetrance of HCM and the short- and long-term outcomes of clinical screening and predictive genetic testing of child relatives of patients with HCM.

Methods And Results: Ninety probands and 361 relatives were included in a family screening program for HCM (1994-2001).

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In hypertrophic cardiomyopathy (HC), electrocardiographic (ECG) changes have been postulated to be an early marker of disease, detectable in sarcomere mutation carriers when left ventricular (LV) wall thickness is still normal. However, the ECG features of mutation carriers have not been fully characterized. Therefore, we systematically analyzed ECGs in a genotyped HC population to characterize ECG findings in mutation carriers (G+) with and without echocardiographic LV hypertrophy (LVH), and to evaluate the accuracy of ECG findings to differentiate at-risk mutation carriers from genetically unaffected relatives during family screening.

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Objectives: Reports of long-term survival and the risk of sudden cardiac death (SCD) after percutaneous transluminal septal myocardial ablation (PTSMA) in patients with hypertrophic obstructive cardiomyopathy (HOCM) are sparse.

Design: Survival and SCD in 77 PTSMA-treated patients (follow-up 3.5 ± 2.

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Background: Single-center reports on percutaneous transluminal septal myocardial ablation (PTSMA) in patients with hypertrophic obstructive cardiomyopathy have shown considerable differences in outcome.

Methods And Results: We report the long-term outcome of 313 PTSMA procedures performed in 279 patients with hypertrophic obstructive cardiomyopathy aged 59±14 years from 1999 to 2010 in 4 Scandinavian centers. Sixty-nine percent of patients had ≥1 comorbidity at baseline.

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Mutations in the Lamin A/C gene (LMNA) are a new part of the spectrum of genes responsible for sudden cardiac death (SCD). Relatives of SCD-cases should receive counselling, clinical assessment and perhaps molecular screening. The consequence of being an LMNA mutation carrier is discussed with regard to counselling and prophylactic measures.

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Aims: Fabry disease, an X-linked storage disorder caused by defective lysosomal enzyme alpha-galactosidase A activity, may resemble sarcomere-gene-associated hypertrophic cardiomyopathy (HCM). The 'cardiac variant' of Fabry disease which only affects the heart may be missed unless specifically tested for.

Methods And Results: We evaluated 90 consecutively recruited HCM probands and their relatives.

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Aims: Several methods are used to induce latent left ventricular outflow tract (LVOT) gradients in patients with hypertrophic cardiomyopathy (HCM). We compared LVOT gradients induced by Valsalva manoeuvre (VM) and exercise echocardiography (EE) in patients with HCM treated with percutaneous transluminal septal myocardial ablation (PTSMA).

Methods And Results: Left ventricular outflow tract gradients were measured at rest, during VM, and during EE in 57 patients 3.

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Background: Genetic testing identifies sarcomere mutation carriers (G+) before clinical diagnosis of hypertrophic cardiomyopathy (HCM), allowing characterization of initial disease manifestations. Previous studies demonstrated that impaired relaxation develops before left ventricular hypertrophy (LVH). The precise impact of sarcomere mutations on systolic function in early and late disease is unclear.

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The American Heart Association (AHA) recommends family screening for hypertrophic cardiomyopathy (HCM). We assessed the outcome of family screening combining clinical evaluation and screening for sarcomere gene mutations in a cohort of 90 Danish HCM patients and their close relatives, in all 451 persons. Index patients were screened for mutations in all coding regions of 10 sarcomere genes (MYH7, MYL3, MYBPC3, TNNI3, TNNT2, TPM1, ACTC, CSRP3, TCAP, and TNNC1) and five exons of TTN.

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