Next Issue
Volume 12, 12
Previous Issue
Volume 12, 10
 
 
cardiovascmed-logo

Journal Browser

Journal Browser
Cardiovascular Medicine is published by MDPI from Volume 28 Issue 1 (2025). Previous articles were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence, and they are hosted by MDPI on mdpi.com as a courtesy and upon agreement with Editores Medicorum Helveticorum (EMH).

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

  • Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
  • You may sign up for e-mail alerts to receive table of contents of newly released issues.
  • PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Reader to open them.
Order results
Result details
Select all
Export citation of selected articles as:
2 pages, 242 KB  
Interesting Images
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
Viewed by 29
Abstract
Ein 50-jähriger Patient wird zugewiesen mit Verdacht auf epileptischen Anfall [...] Full article
Show Figures

Figure 1

2 pages, 235 KB  
Case 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
Viewed by 36
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 [...] Read more.
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
Show Figures

Figure 1

2 pages, 697 KB  
Case 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
Viewed by 38
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
Show Figures

Figure 1

8 pages, 462 KB  
Editorial
Rauchen und Kardiovaskuläre Erkrankungen
by Hugo Saner
Cardiovasc. Med. 2009, 12(11), 305; https://doi.org/10.4414/cvm.2009.01456 - 13 Nov 2009
Viewed by 27
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 [...] Read more.
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
Show Figures

Figure 1

4 pages, 273 KB  
Review
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
Viewed by 41
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 [...] Read more.
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
Show Figures

Figure 1

7 pages, 127 KB  
Review
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
Viewed by 34
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 [...] Read more.
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
Show Figures

Figure 1

Previous Issue
Next Issue
Back to TopTop