Centennial of the original description of Mobitz type II second-degree atrioventricular block.

The year 2024 marks the centenary of Mobitz's description of type II second-degree atrioventricular block. Its definition remains valid to this day with only minor modification for the diagnosis of infranodal conduction block. Mobitz a century ago indicated that his type II atrioventricular block was associated with Stock-Adams attacks and a prolonged duration of the QRS complex before the eventual description of bundle branch block.

Pseudo-2:1 bundle branch block. "Fusion causes confusion".

The fusion of narrow-QRS sinus-generated beats with end-diastolic ventricular extrasystoles occurring in bigeminy can produce an electrocardiographic pattern difficult to differentiate from parasystole. Such an ECG should not be interpreted as 2:1 RBBB because of the variability of the PR intervals.

Incomplete (partial) left anterior hemiblock.

This report describes two electrocardiograms (ECGs) showing unusual manifestations of left anterior hemiblock (LAH). One revealed different degrees of incomplete LAH and the other documented the occurrence of 2:1 LAH. Understanding different degrees of LAH helps to interpret the ECG with regard to intraventricular conduction disorders and other ECG abnormalities.

Sensing of concealed ventricular extrasystoles by pacemakers. Fifty years later.

Whether a pacemaker can sense concealed ventricular extrasystoles still remains debatable since its occurrence was first proposed in 1972. It must remain a diagnosis of exclusion if it really exists. Isoelectric complexes and all the causes of oversensing especially discrete false signals generated by a defective pacemaker lead must be excluded before concealed ventricular extrasystoles can be postulated.

Transient loss of atrial capture: the "atrial pacemaker stunning" phenomenon.

Atrial loss of capture in the chronic phase after implantation may be permanent due to various causes, e.g. technical lead problems or increased scar tissue formation around the lead tip. However, it may also be transient after atrial ischemia in the context of occlusion of the right coronary artery. In this case, it may be preferable to wait for recovery, which may take up to 45 days, instead of immediately performing an atrial lead revision.

Definitions and Pitfalls in the Diagnosis of Atrioventricular Block.

The widespread use of disparate definitions of atrioventricular block has created important diagnostic problems. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation. This review focuses on the clinical importance of the definitions in the diagnosis of the various types of atrioventricular (AV) block and the associated diagnostic pitfalls.

Mobitz type II second-degree atrioventricular block during sleep: true or false?

A number of publications have claimed that Mobitz type II second-degree atrioventricular (AV) block can occur during sleep apnea. None has provided a definition of type II block used in the articles, and representative electrocardiograms have been generally missing. Despite these reports, the existence of type II AV block during sleep must remain questionable.

Unusual manifestation of atypical type I second degree atrioventricular block.

A 25 year-old woman exhibited atypical type I second degree atrioventricular block characterized by constant PR intervals except the PR interval of the beat after the block. This was attributed to vagally induced AV block with failure of the vagal effect to depress the sinus node.

Problematic definitions of Mobitz type II second degree AV block: Historical aspects.

Problems with the definition of type II second degree AV block are best understood by reviewing the historical aspects that include Mobitz's original description, the contributions of the Chicago Arrhythmia School and the growing importance of excluding slowing of the sinus rhythm.

Triple atrial sensing during cardiac resynchronization.

This report describes a patient who underwent cardiac resynchronization complicated by a Twiddler syndrome. This caused triple atrial sensing and an inappropriate shock.

Diagnosis of slow ventricular tachycardia by cardiac resynchronization devices utilizing a desynchronization detection algorithm.

Some cardiac resynchronization therapy (CRT) devices equipped with left ventricular (LV) sensing can develop a specific desynchronization rhythm. Contemporary BIOTRONIK devices are designed with an algorithm called "CRT pacing interrupt" exclusively designed to record the occurrence of the specific form of desynchronization. We report six patients in whom the CRT pacing interrupt function permitted the diagnosis of slow ventricular tachycardia (VT). Slow VT was defined as slower than the programmed VT intervention rates. Although the CRT pacing interrupt function is not designed to detect slow VT, certain episodes of the CRT pacing interrupt function were falsely interpreted by the device as a desynchronization arrhythmia, and the recordings then provided data consistent with the presence of slow VT. The CRT pacing interrupt algorithm permitted a diagnosis of slow VT irrespective of the relationship of LV upper rate interval and cycle length of slow VT.

Apparent dual exit pathways during ventricular tachycardia recorded by an ICD.

Ventricular tachycardia (VT) with dual exit pathways has been demonstrated in many ways. In this respect we found suggestive evidence of dual exit behavior during VT in a patient with an implanted cardioverter-defibrillator. The evaluation was done with continuous recordings of the right ventricular (RV) and left ventricular (LV) electrograms. The recordings documented the varying duration of the LV to RV delay and no change in the RV rate during increases in the LV-RV delay. The unchanged rate ruled out RV participation in the VT circuit. This ruled out the presence of VT with dual exit pathways and provided proof of an unusual RV bystander that did not participate in the VT circuit.

Left ventricular inhibition during cardiac resynchronization caused by sensed left-sided ventricular premature complexes.

A recently published case documented left ventricular (LV) inhibition of a Boston Scientific device by a premature complex (VPC) that was undetected by the right ventricular channel. We have observed a similar response in two patients with a BIOTRONIK cardiac resynchronization device also designed with LV sensing. A spurious response simulating that of the two true cases was also observed in a third patient with a defective LV lead which created isolated false signals. The responses of the BIOTRONIK devices were identical to that of the previously reported findings with the Boston Scientific device. The observations provide insight into the timing function of cardiac resynchronization devices designed with LV sensing.

The QR-max index, a novel electrocardiographic index for the determination of left ventricular conduction delay and selection of cardiac resynchronization in patients with non-left bundle branch block.

Non-left bundle branch block (non-LBBB) remains an uncertain indication for cardiac resynchronization therapy (CRT). Non-LBBB includes right bundle branch block (RBBB) and non-specific LV conduction delay (NSCD), two different electrocardiogram (ECG) patterns which are not generally considered to be associated with LV conduction delay as judged by the invasive assessment of the Q-LV interval. We evaluated whether a novel ECG interval (QR-max index) correlated with the degree of LV conduction delay regardless of the type of non-LBBB ECG pattern, and could, therefore, predict CRT response. In 173 non-LBBB patients on CRT (92 NSCD, 81 RBBB), the QR-max index was measured as the maximum interval from QRS onset to R-wave offset in the limb leads. The correlation between QR-max index and Q-LV interval and the impact of the QR-max index on time to first heart failure hospitalization during 3-year follow-up were assessed. Q-LV correlated better with the QR-max index than with QRSd, particularly in the RBBB group (r = 0.91; p < 0.001 vs. r = 0.19; p < 0.089), while the correlations were r = 0.79 (p < 0.01) and r = 0.68 (p < 0.01), respectively, in the NSCD group. In both groups, the QR-max index was significantly more able than QRSd to identify CRT responders (AUC 0.825 vs. 0.576; p = 0.0008 in RBBB; AUC 0.738 vs. 0.701; p = 0.459 in NSCD). A QR-max index exceeding a cutoff value of 120 ms was associated with CRT response, with predictive values of 86.8 and 81.4% in RBBB and NSCD, respectively. The QR-max index reflects the degree of LV electrical delay regardless of QRS duration in RBBB and NSCD patients and is a useful indicator of suitability for CRT in non-LBBB patients.

Termination of desynchronization rhythm and restoration of cardiac resynchronization by left-sided ventricular premature complexes.

Cardiac resynchronization devices that sense left ventricular (LV) activity and can detect interruptions of resynchronization therapy are able to record all forms of desynchronization rhythms, which are triggered by misalignment of LV timing cycles. We report five cases of this desynchronization rhythm that were terminated by isolated left-sided ventricular premature complexes (LVPC) undetected by the right ventricular (RV) channel and unaccompanied by changes in the duration of the RV pacing cycles. In three cases, the devices did not even sense the LVPCs responsible for desynchronization termination. The restoration of resynchronization in our cases is in contrast to the traditional termination mode that is invariably associated with changes in the duration of the RV cycles.

Interruption of cardiac resynchronization therapy triggered by the automatic right-ventricular pacing threshold test.

We report on three patients with heart failure and left bundle branch block who received a BIOTRONIK implantable defibrillator with resynchronization therapy which manifested loss of resynchronization only at a specific time of the night. Desynchronization was sudden and repeatedly initiated by the daily automatic right ventricular pacing threshold test. Loss of resynchronization occurred after switching back from the temporary test mode to the permanent biventricular pacing mode due to the reactivation of the left ventricular (LV) control of the timing cycles. LV sensed events prevented the emission of an LV paced event by virtue of a realigned LV upper rate interval, thus inhibiting LV pacing.

Hyperkalemia Induced by the Sequential Administration of Metoprolol and Carvedilol.

This report describes the occurrence of asymptomatic hyperkalemia induced by the sequential administration of metoprolol and carvedilol in an 81-year-old man with type II diabetes and stable stage III renal insufficiency. The potassium level rose to 5.6-5.7 mEq/L with metoprolol and normalized when the agent was discontinued. However, the potassium level rose again to 5.6 mEq/L after the administration of carvedilol but the level normalized by halving the dose. The observations of hyperkalemia induced by two different ß-blocker drugs in the same patient confirm that this side effect is common to all ß-blocker drugs.