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Resetting responses and response to entrainment have confirmed the reentrant nature of flutter and established the presence of a fully excitable gap in the majority of patients. During atrial flutter, the use of 3D electroanatomic mapping studies and the entrainment pacing technique have aided in defining the mechanism of the arrhythmia with the activation sequence, providing information regarding the timing of intra-atrial events with respect to the surface electrocardiogram, especially for the non-CTI-dependent form and for left flutter.

Further study will be needed, however, to definite the precise boundaries of flutter and to better identify correlations between the location of the different electrophysiologic types of reentrant circuits and their electrocardiographic characteristics.

The literature on ablation for AF has many of the features of clinical research in the era preceding evidence-based medicine and randomised trials. Many studies emanate from single centres, involve low patient numbers, and fail to provide adequate statistical analysis, including intention to treat analysis and evaluation of statistical power. As was the case with Maze operations, new procedures are continually proposed without completing satisfactory evaluations of previously proposed procedures. Very worrisome is that most studies have not involved neutral committees for the recording and supervision of severe complications.

The belief that AF ablation now represents a standard or, indeed, first-line treatment is excessively optimistic and may reflect occupational and economic factors encouraging mechanistic invasive procedures.

Atrial and dual defibrillators held great promise when they were introduced in the 1990s.

The devices are effective and safe in selected patients. Tolerability and acceptance by patients is good in the short term but only moderate in the longer term. The complication rate is relatively low. However, advances in ablation techniques for the treatment of atrial fibrillation have limited and will continue to limit the use of implantable atrial defibrillators. In combination with ICDs they may find a continued role in a patient group that should be further defined.

Patients with right ventricular pacing and heart failure may be candidates for resynchronisation therapy with the upgrading to biventricular pacing.

The procedure has been shown to be simple and safe. In addition, the results of the above-mentioned studies are encouraging and show that upgraded patients may profit from a better quality of life. However, the life expectancy of these patients remains to be investigated.

As discussed above, the more frequently the RV apex is paced, the more likely cardiac performance will be compromised. This explains why, although maintenance of AV synchrony afforded by conventional DDDR is intuitively superior to VVIR, this has been surprisingly difficult to prove. Large randomised clinical trials have reached a consensus that there is no survival benefit in patients conventionally DDDR paced; furthermore, DDDR pacing may be associated with an increased risk of death among ICD patients.

These trials have highlighted the importance of developing sophisticated pacemakers and ICDs capable of minimising, in patients without AV block, RV pacing, thus preserving normal ventricular activation while providing physiologic pacing support.

A reliable alternative to RV pacing may well be biventricular pacing, which seems to be a valid option to preserve LV function in patients who present with LV dysfunction and heart failure symptoms. In addition, there is the option to use CRT for ‘primary prevention’ in selected patients who require ventricular pacing for electrical reasons.

New-onset AF and associated stroke were significantly reduced by losartan-based compared with atenolol-based antihypertensive treatment, with similar blood pressure reduction, as shown in the LIFE study. The antiarrhythmic effect of losartan was, in multivariate analysis, similar to that of a 30 mmHg difference in systolic blood pressure.

Atrial fibrillation in AMI is often secondary to other post-AMI complications, but is itself an independent predictor of a worse outcome. AF can be prevented by optimising the treatment of AMI with reperfusion therapy, beta-blockers, and ACE inhibitors. When AF occurs, it should be treated with DC shock as soon as possible and/or drugs with little haemodynamic impact according to the clinical status.

Available evidence supports the hypothesis that CRT results in favourable structural and electrical remodeling. Whether this effect would obviate the need for back-up defibrillation capability in CRT devices is unclear and should be the focus of further studies.

Atrial flutter may occur as a complication of PCI, but most of the time the Patients’ characteristics play important roles in the occurrence of this type of arrhythmia. For instance, ongoing acute MI can be the real reason for AF. Generally, AF tends to revert spontaneously, but when necessary treatment must be given promptly. If the patient is compromised by ventricular rate or by the loss of atrial contribution to cardiac output, synchronised DC cardioversion should be performed without delay. Intravenous beta-blockade can be effective for acute rate control. Calcium-channel blockers can be administered to promptly control ventricular rate. Digoxin, amiodarone and dofetilide are the drugs of choice for treating patients with acute MI with heart failure.

In the present animal model study, the pacemaker Sophós 100 proved fully reliable in a 1 month follow-up period. TVI sensor operation did not interfere with conventional pacemaker functions, opening the way to its implantation in human beings.