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Congress report: World Congress of Cardiology, 2012

Congress report: World Congress of Cardiology, 2012
  • Cardiometabolic
  • Hypertension


Resource type



Sudden cardiac death (SCD)
Mechanisms of sudden cardiac death
Epidemiology of sudden cardiac death
Infective endocarditis
Surgical management of infective carditis

A report from the World Congress of Cardiology, 2012, Dubai, United Arab Emirates, 18-20 April, 2012.

Two topics of discussion at the recent World Congress of Cardiology are of particular importance when considering hypertension. Professor Omar Salah Awwad brings us the latest on sudden cardiac death and infectious endocarditis.

Sudden cardiac death
Sudden cardiac death (SCD) is a condition defined as unexpected natural death due to cardiac cause within a short period from the onset of symptoms in a person without any prior condition that would appear fatal.

It was stated that the vast majority of patients who have experienced SCD have had cardiac structural abnormalities. In the adult population, these consist predominantly of coronary heart disease, cardiomyopathies, valvular heart disease and abnormalities of the conduction system. Discussion also explored the role of tachy-arrhythmias versus brady-arrhythmias in sudden cardiac death, the electrophysiological effects of ischemia, through induction of rapid polymorphic ventricular tachycardia and ventricular fibrillation and the role of the autonomic nervous system in the genesis of arrhythmias by creating refractories and/or conduction disturbances.

One presentation noted that SCD accounts for 400,000 deaths per year in the US.  When its definition is restricted to death within less than 2 hours from onset of symptoms, 12 percent of all natural deaths are sudden, and 88 percent of these are due to cardiac causes. The WHO has reported an annual incidence of SCD of 1.9 per 1000 persons in men and 0.6 in women, again accounting for nearly half the deaths from coronary heart disease (CHD).

Evaluation of patients
Another presentation emphasised the importance of establishing the underlying cardiac pathology and excluding the possibility of acute myocardial infarction. Again, the differentiation between primary cardiac arrest due to acute circulatory or respiratory failure and secondary cardiac arrest due to underlying cardiac disease was stressed.

The treatment for patients at risk for SCD can be divided it into pharmacological and non-pharmacological therapy.

In considering pharmacological therapy, speakers mentioned the role of beta blockers as the best established and effective therapy especially in patients with CHD. Angiotensin converting enzyme inhibitors are highly effective treatments in patients with heart failure as they have a powerful effect on mortality.

It was stated that the use of anti-arrhythmic drugs in the treatment of SCD is disappointing generally but it was mentioned that only amiodarone and dofetilide can have a role in this situation.

Non-pharmacological therapy can include coronary surgery such as coronary artery bypass graft (CAPG) in patients with CHD.

Implantable defibrillators were presented as effective and potent methods against both tachycardiac and bradycardiac SCD regardless the underlying heart disease or various triggers of arrhythmias.

Infective endocarditis
Infective endocarditis (IE) was discussed in two important presentations.

The changing epidemiology
The spectrum of IE continues to change. There are approximately 10,000 to 15,000 cases annually in the US. The median age of patients has increased from an average of 30 years of age in 1926 to over 50 currently. Degenerative valve disease and mitral valve prolapse have replaced rheumatic heart disease as the most common substrate for IE and, moreover, the number of children with congenital heart disease surviving into adulthood has increased the improved palliative and corrective surgical procedures.

The use of IV drugs is also associated with a high risk of IE. Multiple routes of transient bacteremia from poor sterile techniques and contaminated drug material commonly lead to right-sided valvular infections. New bio-prosthetic material to correct congenital and acquired valvular disease has predisposed many patients with prosthetic heart valves to the risk of IE.

A growing number of patients have no identifiable cardiac lesions. Most of those patients are above 65 years of age and probably have degenerative changes that serve as a nucleus for the initiation of IE. Nosocomial infections due to intravenous devices as catheters as well as procedures involving the gastrointestinal and genitourinary tracts may facilitate development of the causal bacteremia in this group. Other susceptible populations include patients with immunosuppression (HIV) and those who have undergone organ transplantation.

Surgical management
Despite the availability of potent antimicrobial therapy, surgical intervention is needed for approximately one third of the cases of IE. Indeed, prosthetic valve endocarditis and fungal infections are difficult to eradicate with antibiotics alone.

Moreover, when IE is complicated by valvular regurgitation and chronic heart failure, surgical therapy should be undertaken regardless of the duration of antibiotic therapy. If the patient is hemodynamically stable, the indication for and timing of surgery are not as clear. When feasible, it is recommended that optimal antimicrobial therapy be given for several days to eradicate or reduce the bacteremia prior to surgical intervention.          

Recommendation for surgery


  • Acute aortic or mitral valve regurgitation with heart failure
  • Evidence of peri annular abscess or peri valvular extension
  • Fungal endocarditis
  • Suppurative  pericarditis  
  • Prosthetic valve dysfunction
  • Early prosthetic valve endocarditis (within 60 days after surgery)            


  • Recurrent emboli after appropriate antibiotic therapy
  • Persistent bacterimia despite appropriate antibiotic therapy
  • Enlarging vegetations
  • Repeated relapses
  • Infection with gram negative organisms


  • Mobile vegetations > 10 mm


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