Expert consensus document on automated diagnosis of the electrocardiogram: The task force on automated diagnosis of the electrocardiogram in Japan part 3: Inappropriate internal processing in the automatic diagnosis of electrocardiograms and its problems.

Computer diagnosis of electrocardiograms is widely used to provide useful information in clinical practice and medical checkups. However, it is common for users to be confused by the inappropriate diagnosis. We illustrate some examples of inappropriate automatic diagnoses and discuss the actual situation of inappropriate automatic processing and its problems.

Expert consensus document on automated diagnosis of the electrocardiogram: The task force on automated diagnosis of the electrocardiogram in Japan: Part 2: Current status of inappropriate automated diagnosis is widely used electrocardiographs in Japan.

It is important to objectively grasp the current status of automated electrocardiogram (ECG) diagnosis. This report aimed to analyze and evaluate ECG records that our members have encountered as an inappropriate diagnosis in real-world clinical practices.

Expert consensus document on automated diagnosis of the electrocardiogram: The task force on automated diagnosis of the electrocardiogram in Japan. Part 1: Nomenclature for diagnosis and abnormal findings.

As these terms should accurately represent the abnormal findings and conditions as much as possible, we propose to unify these terms into terminologies that are not confusing and easy to understand for everyone.

Long-term effects of upstream therapy on paroxysmal atrial fibrillation in patients without overt heart diseases.

Most paroxysmal atrial fibrillation (PAF) ultimately becomes chronic atrial fibrillation (CAF), even in the presence of antiarrhythmic drugs. Upstream therapies such as calcium channel blockers (CCB), angiotensin-converting enzyme inhibitors (ACEI), or statins have attracted attention for treating AF patients. We have previously reported that ACEI inhibited the progression of PAF to CAF. CCB and statins were also reported to inhibit the development of AF, but the follow-up periods in several of the papers appeared to be too short to allow a clear verdict on the antiarrhythmic effects. We therefore conducted a retrospective analysis of the relationship between long-term treatment (over 5 years) with an ACEI, CCB, or statin and outcome in patients with PAF (n = 125).The follow-up period was 7.7 +/- 3.1 years. Class I antiarrhythmic drugs were prescribed for 76.6% of the patients, ACEI for 36.0%, CCB for 47.2%, and statins for 20.0%. We assessed the cardiac rhythm from the medical records or electrocardiograms and determined the time from the first visit to the development of CAF. Kaplan-Meier analysis showed that the use of an ACEI significantly decreased the cumulative probability of CAF, while class I antiarrhythmics, CCB, and statins did not inhibit progression to CAF. Multivariate analysis showed that only ACEI was related to a reduced progression to CAF (odds ratio, 0.112; 95% confidence interval, 0.034 to 0.374, P = 0.001). Class I antiarrhythmic drugs, CCBs, and statins showed no such association.ACEI thus appear to be superior to CCB or statins with respect to upstream therapy.

Inhibition of the reverse mode of the Na+/Ca2+ exchange by KB-R7943 augments arrhythmogenicity in the canine heart during rapid heart rates.

To test the hypothesis that the reverse mode of the Na+/Ca2+ exchange augmented by a rapid heart rate has an antiarrhythmic effect by shortening the action potential duration, we examined the effects of KB-R7943 (2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl] isothiourea methanesulfonate), a selective inhibitor of the reverse mode of the Na+/Ca2+ exchange, to attenuate this effect. We recorded the electrocardiogram, monophasic action potential (MAP), and left ventricular pressure in canine beating hearts. In comparison to the control, KB-R7943 significantly increased the QTc value and MAP duration. MAP alternans and left ventricular pressure alternans were observed after changing the cycle length to 300 milliseconds in the control studies. KB-R7943 magnified both types of alternans and produced spatially discordant alternans between right and left ventricles. Early after-depolarizations and nonsustained ventricular tachycardia occurred in the presence of KB-R7943. Our data suggest that the reverse mode of the Na+/Ca2+ exchange may contribute to suppression of arrhythmias by abbreviating action potential duration under pathophysiological conditions. This conclusion is based on further confirmation by future studies of the specificity of KB-R7943 for block of the reverse mode of the Na+/Ca2+ exchange.

Angiotensin-converting enzyme inhibitor therapy inhibits the progression from paroxysmal atrial fibrillation to chronic atrial fibrillation.

BACKGROUND: Atrial fibrillation is a progressive disease, which in the paroxysmal form (PAF) becomes more frequent and finally becomes chronic (CAF). A retrospective analysis of patients with PAF was conducted to examine the hypothesis that angiotensin-converting enzyme inhibitors (ACEI) will prevent the progression to CAF. METHODS AND RESULTS: On the basis of their treatment, 95 patients with PAF were divided into 2 groups: 42 patients treated with ACEI for hypertension throughout the period of treatment and follow-up (ACEI group) and 53 patients not given ACEI (non-ACEI group). Cardiac rhythms were assessed either from the medical records or the electrocardiograms recorded every 2-4 weeks at follow-up visits. The mean follow-up time was 8.3+/-3.5 years. There was no significant difference in the use of antiarrhythmic drugs, left atrial diameter or left ventricular ejection fraction between the 2 groups. The Kaplan-Meier curve for the time to occurrence of CAF showed a lower incidence of CAF in the ACEI group and demonstrated that the 5-year probability for persistence of PAF without progression to CAF was 88.3%, but 47.5% in the non-ACEI group. CONCLUSIONS: These results indicate that ACEI will prevent progression from PAF to CAF.

On the mechanism of the probabilistic nature of ventricular defibrillation threshold.

The probabilistic nature of the ventricular defibrillation threshold (DFT) remains poorly understood. We hypothesized that shock outcome is a function of the amount of myocardium in its vulnerable period (VP). The endocardial surface of five isolated, perfused swine right ventricles was mapped with 477 bipolar electrodes during ventricular fibrillation (VF). Shock parameters and VF cycle length were not significantly different in the successful (S; n = 26) and failed (F; n = 26) trials. At the instant of the shock, the number of sites with 45- to 55-ms recovery was significantly smaller in the S trials than the F trials (P < 0.04). No significant difference in the number of sites with recovery intervals outside the 45- to 55-ms range was seen in S and F shocks. Endocardial action potential showed that a recovery time of 45-55 ms corresponded to the VP spanning -15 to -60 mV in 92% of the regenerative action potentials. We conclude that the probabilistic nature of the DFT is related to the amount of myocardium in its VP.