Mitral valve palpitations

Few disorders ever provoked more interest and controversy than mitral valve prolapse (MVP). Past echocardiographic over-diagnosis led to it becoming a whipping boy for otherwise unexplained chest pain, palpitation, arrhythmias and emboli. Surgical centres reported a high incidence of endocarditis and severe regurgitation. Most investigators who have studied the prevalence of arrhythmias in MVP have concluded that they are more common in this syndrome than in the general population and that there is a causal rather than a fortuitous relationship. However, the prevalence of arrhythmias in reported studies is probably higher than in unselected MVP patients. Multiple ventricular premature beats, ventricular tachycardia and sudden death have been reported. Suggested mechanisms have included a focal cardiomyopathy with incoordinate contraction and relaxation, QRS dispersion, a long QT, traction on papillary muscles by prolapsed leaflets, interference with the blood supply of the papillary muscles, stimulation of the endocardium by the chordae and diastolic depolarisation of muscle fibres in redundant leaflets with triggered repetitive automaticity. MVP has been associated with pre-excitation giving rise to atrioventricular re-entry tachycardia. Autonomic dysfunction and a hyperadrenergic state has been claimed and this may also be responsible for supraventricular arrhythmias including atrioventricular nodal re-entry tachycardia, flutter and fibrillation. Electrophysiological studies have yielded contradictory results which may be due to the heterogeneity of the patients studied and variability of the mechanisms. Whatever the true prevalence, arrhythmias in MVP are usually benign. Syncope and sudden death are rare. Anti-arrhythmic therapy is only warranted in patients with frequent and distressing symptoms shown to be due to the arrhythmias or when arrhythmias are judged potentially life threatening. Beta-blockers are particularly helpful in the syndrome.