Cardiovascular Medicine

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Kammertachykardie aus Substrat

by Richard Kobza and Paul Erne

Cardiovasc. Med. 2009, 12(11), 317; https://doi.org/10.4414/cvm.2009.01458 - 13 Nov 2009

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Abstract

Ein 50-jähriger Patient wird zugewiesen mit Verdacht auf epileptischen Anfall [...] Full article

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2 pages, 235 KB

Open AccessCase Report

A Case of Infective Endocarditis Caused by Bartonella Quintana: Prolonged Mild Symptoms and a Sudden Life-Threatening Complication

by Florian S. Schoenhoff, Friedrich S. Eckstein, Stefan Zimmerli and Thierry P. Carrel

Cardiovasc. Med. 2009, 12(11), 315; https://doi.org/10.4414/cvm.2009.01455 - 13 Nov 2009

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Abstract

The morbidity and mortality associated with infective endocarditis can be significantly reduced by early diagnosis and initiation of effective therapy. Due to the often nonspecific prosaic symptoms associated with infective endocarditis, patients are likely to seek initial medical care from their primary care physicians. The authors present the history of a patient suffering from indolent prolonged illness with moderate fever who developed painless macrohematuria and triple valve endocarditis with Bartonella quintana. This pathogen is a gram-negative bacterium responsible for the epidemic louse-borne trench-fever seen in Europe during World War I and particularly seen as an infectious agent in HIV patients. Full article

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2 pages, 697 KB

Open AccessCase Report

New Amplatzer Duct Occluder II for Antegrade Closure of Patent Ductus Arteriosus

by Stéphane Cook, Tobias Rutz and Bernhard Meier

Cardiovasc. Med. 2009, 12(11), 313; https://doi.org/10.4414/cvm.2009.01457 - 13 Nov 2009

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Abstract

Transcatheter closure of patent ductus arteriosus is a safe and effective technique. The new version of the Amplatzer PDA occluder (Amplatzer Duct Occluder II) permits antegrade delivery and significantly simplifies the procedure. Full article

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8 pages, 462 KB

Open AccessEditorial

Rauchen und Kardiovaskuläre Erkrankungen

by Hugo Saner

Cardiovasc. Med. 2009, 12(11), 305; https://doi.org/10.4414/cvm.2009.01456 - 13 Nov 2009

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Abstract

The causative relationship between smoking and coronary heart disease is well established, with relative risks (RRs) or odds ratios (ORs) estimated at 1.5–3 or higher. The pathophysiologic mechanisms of vascular damage from smoking include changes of haemostatic factors with increased coagulation and clotting tendency, endothelial dysfunction, increase of heart rate and blood pressure, decrease of heart rate variability, increase of arterial stiffness, increase of inflammatory markers, oxydative damage, negative influence on serum lipids and in particular decrease of HDL cholesterol. Smoking has also a negative influence on the course of disease in various cardiovascular situations and after interventions; these include increased mortality after PTCA for smokers at the time of intervention, increased morbidity and mortality in patients with leftventricular dysfunction, supraventricular and ventricular rhythm disturbances in patients after IC implantation and increased risk of sudden death in patients with coronary disease. Young women are particularly susceptible to vascular damage with an up to 14–fold increase of risk for myocardial infarction when smoking 20–39 cigarettes per day. The combination of smoking with the use of anticonceptive drugs further increases the cardiovascular risk considerably. Negative influences of smoking on endothelial function vary only slightly between light and heavy smokers. The same is true for haemodynamic effects and negative effects on the autonomic nervous system. Observational studies have shown that smoking cessation decreases the risk for cardiovascular events and mortality in patients with coronary heart disease up to 50%. A systematic review from the year 2003 shows a 36% reduction of mortality in patients with coronary disease who quit smoking in relation to those who continue to smoke (RR = 0.64; 95%-CI= 0.58–0.71). Smoking is the most important single cardiovascular risk factor. The fact that during the last 25 years cardiovascular mortality decreased by around 50% in most western European countries can be attributed by almost 50% to a decrease in smoking. Therefore all efforts to increase awareness for the negative effects of smoking on the cardiovascular system and the need to support smoking cessation in smokers are of great importance. In this regard, the efforts of the Swiss Heart Foundation in cooperation with Cardiovasc Swiss to increase awareness for the importance of smoking and smoking cessation for cardiovascular disease merit strong support from all persons working in the field of cardiovascular disease prevention, treatment and rehabilitation. Full article

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4 pages, 273 KB

Open AccessReview

Knöchelödeme—Nicht Alle Dihydropyridin-Kalziumantagonisten Sind Gleich Beschaffen

by Franz H. Messerli and Ehud Grossman

Cardiovasc. Med. 2009, 12(11), 301; https://doi.org/10.4414/cvm.2009.01461 - 13 Nov 2009

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Abstract

Pedal oedema is a common dose dependent adverse effect of dihydropyridine calcium antagonists. Pathogenetic mechanisms leading to pedal oedema are related to a calcium antagonist induced paresis of the precapillary sphincter resulting in intracapillary hypertension. Intracapillary hypertension increases capillary permeability and facilitates oedema formation. Longstanding pedal oedema can lead to hyperpigmentation and dyspigmentation. Calcium antagonist induced pedal oedema is more common in women than in men and increases with age. Recent studies have documented that not all dihydropyridine calcium antagonists are created equal with regard to pedal oedema. For a given fall in blood pressure, lercanidipine and lacidipine are associated with lesser pedal oedema than is amlodipine. The pedal oedema associated with calcium antagonist does not respond well to diuretic therapy since it is not directly caused by sodium retention. The addition of a blocker of the renin angiotensin system (ACE inhibitor, angiotensin receptor blocker, direct renin inhibitor) by opening the post capillary sphincter diminishes intracapillary pressure and therefore has a mitigating effect on the calcium antagonist induced pedal oedema. Full article

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7 pages, 127 KB

Open AccessReview

Management of Acute Heart Failure

by Ayesha Hasan and William T. Abraham

Cardiovasc. Med. 2009, 12(11), 294; https://doi.org/10.4414/cvm.2009.01459 - 13 Nov 2009

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Abstract

Heart failure presents a substantial dilemma in the United States and Europe with a high prevalence and a persistent rise in admissions for acute episodes despite recent advances in the field. Evidence-based pharmacologic therapy has been well established in chronic heart failure, but acute management of decompensated heart failure is largely empiric. More trials are emerging regarding such treatment options. Inpatient treatment focuses on improving congestive symptoms and hemodynamics, avoiding renal dysfunction, treating reversible causes/comorbidities, and initiating evidence-based therapy prior to discharge. Pharmacologic management of acute heart failure episodes are reviewed, including investigational therapies. Full article

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Cardiovasc. Med., Volume 12, Issue 11 (11 2009) – 6 articles

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