Cardiovascular Medicine

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Open AccessCommunication

20 Jahre Kardiologie am UniversitätsSpital Zürich, 1996–2016

by Thomas F. Lüscher

Cardiovasc. Med. 2017, 20(2), 51; https://doi.org/10.4414/cvm.2017.00457 - 15 Feb 2017

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Abstract

Die Zeit vor 1996 Gewiss, Herzmedizin wurde bereits vor 1996 in Zürich betrieben (Abb. 1) [...] Full article

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5 pages, 4589 KB

Open AccessCase Report

Lamin A/C Cardiomyopathy: Case Report and Review of the Literature

by Carmen Schneiders, Marcello Di Valentino, Argelia Medeiros-Domingo, Rolf Wyttenbach and Andrea Menafoglio

Cardiovasc. Med. 2017, 20(2), 46; https://doi.org/10.4414/cvm.2017.00458 - 15 Feb 2017

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Abstract

A 45-year-old man known for bradycardia underwent cardiac evaluation because of complete atrioventricular block. His mother underwent heart transplantation at the age of 60 for dilated cardiomyopathy. Echocardiography revealed mild left ventricular dilatation, and a subnormal left ventricular ejection fraction (LVEF) of 50% due to septal hypokinesia. Cardiac magnetic resonance imaging showed linear mid-myocardial late gadolinium enhancement of the basal septum, indicating myocardial fibrosis. We decided to implant a dual chamber pacemaker programmed in DDD modality. On the basis of the clinical history we suspected a lamin A/C (LMNA) mutation cardiomyopathy. A known pathogenic heterozygote mutation c.1129C>T (p.Arg377His) in the LMNA gene was identified, confirming the diagnosis of LMNA cardiopathy. At this time we suggested an upgrade to an implantable cardioverter-defibrillator in order to prevent sudden cardiac death, but the patient refused. Eighteen months after the pacemaker implantation the patient is alive and well. Full article

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8 pages, 630 KB

Open AccessReview

COPD Exacerbation and Prevention

by Carlos Roberto Pérez Valdés, Alexandra Lenoir and Laurent Nicod

Cardiovasc. Med. 2017, 20(2), 38; https://doi.org/10.4414/cvm.2017.00461 - 15 Feb 2017

Cited by 1 | Viewed by 204

Abstract

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality worldwide, therefore representing a major healthcare burden. Exacerbations become more frequent as the severity of disease increases and can lead, through dynamic hyperinflation, to life-threatening respiratory failure. Diagnosis of acutely exacerbated COPD (AECOPD) is based on Anthonisen’s criteria. It is assessed through careful history-taking, observation of clinical signs and consideration of certain laboratory parameters. Differential diagnoses, especially a cardiac origin for the patient’s symptoms, should be excluded. Most COPD exacerbations are associated with viral and bacterial infections. Even though the exact role of the lung microbiome is still subject to debate, we do know that its composition changes during an exacerbation. Several biomarkers for AECOPD, such as percentage of blood eosinophils, are being investigated. Episodes of AECOPD carry an increased risk for cardiovascular events, possibly the consequence of an underlying systemic inflammation. Elevated levels of N-terminal prohormone of brain natriuretic peptide and troponin T predict increased mortality during exacerbations. Coronary angiography is a valuable diagnostic and therapeutic tool in this context. Smoking cessation, influenza and pneumococcal vaccines, optimising therapy (including inhaler technique and treatment with long-acting inhaled bronchodilators) reduce the number of exacerbations. Adding inhaled corticosteroids and phosphodiesterase-4 inhibitors may be of benefit. Pulmonary rehabilitation reduces the risk of rehospitalisation after a recent exacerbation. Long-term immunomodulation with azithromycin can be used in patients with frequent exacerbations who are nonsmokers. Acute exacerbations of COPD are an important event in the course of the disease, can irreversibly accelerate lung function decline and are associated with significant mortality. Their prevention and treatment is therefore of utmost importance. It has recently become clear that several different phenotypes of COPD patients exist, for stable disease and exacerbations, which could guide optimal therapy in the future. Full article

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2 pages, 471 KB

Open AccessReview

Das Happy-Heart-Syndrom: Positive Emotionen und Takotsubo-Syndrom

by Victoria L. Cammann, Christian Templin and Jelena-R. Ghadri

Cardiovasc. Med. 2017, 20(2), 36; https://doi.org/10.4414/cvm.2017.00460 - 15 Feb 2017

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Abstract

Takotsubo syndrome (TTS) is an underestimated acute heart failure syndrome masquerading as acute myocardial infarction at presentation and mostly affecting postmenopausal women. As TTS is often precipitated by emotional stress especially after negative life events (e.g., grief, anger, fear) the widespread term of the broken heart syndrome was coined. So far the role of positive emotional stress in TTS is less clear. Data from the International Takotsubo Registry (InterTAK Registry, www.takotsubo-registry.com) have demonstrated that happy life events such as becoming a grandmother, son’s wedding, or winning several jackpots can ultimately lead to TTS. These new findings should lead to a paradigm shift in clinical practice as they show that the triggers for TTS can be more diverse than initially thought. These results have recently been published in the European Heart Journal. Full article

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9 pages, 868 KB

Open AccessReview

Ventricular Arrhythmias in Congenital Heart Disease: How Can the Electrophysiologist Help?

by Dipen Shah

Cardiovasc. Med. 2017, 20(2), 27; https://doi.org/10.4414/cvm.2017.00459 - 15 Feb 2017

Cited by 2 | Viewed by 72

Abstract

Patients with congenital heart disease often have ventricular hypertrophy, dilatation and/or fibrosis as part or a direct consequence of their malformation. Moreover, they often have ventricular scars and/or patches and develop secondary haemodynamic overload or valvular abnormalities as a consequence of reparative surgery/interventions that worsen ventricular remodelling. This ventricular remodelling predisposes to polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF) and sudden cardiac death, as in other forms of heart disease. The presence of an extensive ventricular scar/patch leads to the occurrence of rapid and often poorly tolerated sustained monomorphic reentrant VT, resulting in haemodynamic collapse and even sudden cardiac death. Acute therapy of VT/VF is applicable in accordance with standard guidelines. Chronic management includes reparative therapy of the underlying congenital heart malformation and heart failure treatment, but specific arrhythmia management should ideally be provided by a qualified electrophysiologist who can precisely diagnose the arrhythmia and its mechanism, provide prognostic stratification, determine the substrate, administer specialised electrical therapies including antitachycardia pacing and automatic internal cardiac defibrillation from an implanted device, or perform catheter ablation of the VT substrate. Finally, electrophysiological evaluation can provide valuable information to guide the surgeon to incorporate arrhythmia-neutralising incisions into reparative surgery. Full article

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Cardiovasc. Med., Volume 20, Issue 2 (02 2017) – 5 articles

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