Rate-dependent Left Bundle Branch Block Research Articles

Paroxysmal Severe Mitral Regurgitation

ObjectiveTo investigate the clinical presentation, pathophysiology, and treatment for "paroxysmal severe mitral regurgitation" (MR), which is an underappreciated cause of heart failure with preserved left ventricular ejection fraction. MethodsWe retrospectively reviewed cases of transient severe MR that were evaluated at Mayo Clinic in Rochester, Minnesota, between January 1, 2006, and December 31, 2019. Paroxysmal severe MR was defined as the appearance of transient severe MR in patients with mild MR at rest, normal left ventricle (LV) size, left ventricular ejection fraction greater than 40%, and absence of obstructive coronary artery disease. ResultsWe identified 6 patients (5 women) with a median age of 68 years. There were 3 distinct mechanisms of paroxysmal severe MR, which we labeled types 1, 2, and 3. Type 1 MR was caused by LV dyssynchrony from a rate-dependent left bundle branch block, which led to apical leaflet tenting and incomplete coaptation. Type 2 MR occurred from mitral annular dilatation during maneuvers that increased left-sided volume. Type 3 MR was caused by coronary artery vasospasm with apical leaflet tenting. Treatments varied depending on the underlying cause and included cardiac resynchronization therapy for type 1, surgical valve replacement for type 2, and medical therapy for type 3. ConclusionParoxysmal severe MR is a rare cause of heart failure in patients with preserved LV function. We have identified 3 distinct mechanisms that can lead to this dynamic process, with treatments varying based on the underlying cause.

Rate‐dependent aberrancy and cardiac resynchronization therapy

Left bundle branch block (LBBB) can result in significant dyssynchrony in left ventricular (LV) contraction, ultimately leading to cardiac remodeling. LBBB can be rate dependent and may appear with LV systolic dysfunction. Cardiac resynchronization therapy (CRT) has been demonstrated to improve hemodynamics as well as clinical symptoms in patients with LBBB. We describe the case of a 57-year-old man who underwent CRT implantation due to exertional dyspnea, rate-dependent LBBB, and impaired left LV systolic function.

Narrow QRS complexes within left bundle branche block in a patient with chest pain

We present the case of a patient with chest pain, palpitations, atrial fibrillation, left bundle branch block (LBBB) and occasional early narrow QRS complexes. An intracardiac study revealed rate-dependent LBBB with additional hidden rate-dependent slowing in the contralateral bundle branch, resulting in normalization of the early conducted QRS complexes.

Oversensing issues leading to device extraction: When subcutaneous implantable cardioverter-defibrillator reached a dead-end

Subcutaneous implantable cardioverter-defibrillator (S-ICD) implantations are rapidly expanding. However, the subcutaneous detection and interpretation of cardiac signals in S-ICDs is much more challenging than by conventional devices. There is a complete paradigm shift in cardiac signal sensing with subcutaneous signal detection, leading in some cases to oversensing with restricted programming options. The aim of this single-center study was to quantify and describe cases where recurring oversensing made the extraction of the device necessary. Consecutive patients (n = 108) implanted with an S-ICD in our tertiary referral hospital were considered for analysis. Clinical and remote monitoring data were analyzed. The S-ICD had to be explanted in 6 of 108 implanted patients (5.6%) because of refractory oversensing issues: myopotential oversensing, P- or T-wave oversensing, rate-dependent left bundle branch block aberrancy during exercise with R-wave double counting, and R-wave amplitude decrease after ventricular tachycardia ablation leading to noise detection. Seventeen of 108 patients experienced oversensing (15.7%): 9 patients had at least 1 inappropriate charge without a shock (8.3%), 3 patients had at least 1 inappropriate shock (2.8%), and 5 patients had both episodes (4.6%). So far, cardiologists have had to deal with transvenous ICD lead fractures, but signal oversensing without correcting programming option could be the equivalent weakness of S-ICDs, despite an adequate screening.

Rate-dependent left bundle branch block caused by hyperkalaemia.

A 73-year-old male presented to the emergency department with vomiting and diarrhoea. No abnormalities were found on physical examination, besides a blood pressure of 80/40 mmHg. The blood tests showed acute renal insufficiency and a potassium of 9.0 mmol/L (3.5–5.0). The electrocardiogram (ECG) showed atrial fibrillation and the occurrence of a left bundle branch block (LBBB) when the heart rate exceeded 76 beats per minute (Fig. 1). When the heart rate decreased the ECG abnormalities disappeared (Fig. 2). Previous ECGs had never shown LBBB. Fig. 1 Atrial fibrillation and left bundle branch block Fig. 2 Narrow ECG complexes, the left bundle branch block has disappeared

Intraoperative Detection of Rate Dependent Left Bundle Branch Block

Rate dependent left bundle branch block (RDLBBB) is an uncommon case. RDLBBB is defined as an intraventricular conduction defect that may return, if only temporarily, to sinus rhythm at lower heart rates. It appears when the heart rate exceeds a certain critical value. Although RDLBBB is usually benign, its diagnosis and treatment have clinical importance for association of RDLBBB and myocardial ischemia and infarction. Therefore, in the case of detection of intraoperative RDLBBB, a clear differentiation should be done as soon as possible. Also it is important to start appropriate treatment and to do clinical follow-up examination. We report a case of intraoperative RDLBBB during general anesthesia for laparoscopic cholecystectomy in 82 years old female patient who has a history of hypertension.

An Unusual Presentation of Transient Left Bundle Branch Block in a Patient with Acute Pancreatitis: A Case Report

Introduction: New-onset left bundle branch block (LBBB) in the electrocardiogram (ECG) is considered to be a particularly serious condition, which requires prompt further evaluation for the exclusion of possible underlying myocardial ischemia. . Case presentation: A 76 year old female Caucasian patient presented with gradually worsening abdominal discomfort, accompanied by nausea and vomiting. Initial clinical and laboratory investigations were indicative of acute pancreatitis, which was confirmed with an abdomen ultrasonography. A routine ECG, which was performed in the second day of hospitalisation, identified new-onset LBBB morphology, which was not initially present. The possibility of a rate-dependent LBBB was immediately excluded, since no significant alteration of the heart rate was noted. Considering the fact that myocardial infarction among elderly female individuals may present with non-typical features, a serious diagnostic problem appeared. Since there were no echocardiographic or biochemical indications consistent with acute myocardial ischemia it was decided to continue the medical treatment without alterations. The transthoracic echocardiogram also excluded the presence of significant valve lesions or any abnormalities in the structure and function of the myocardium. An ECG was repeatedly performed on a daily basis, but the LBBB persisted until the patient was discharged, seven days after admission, with a diagnosis of acute idiopathic pancreatitis. About three weeks after discharge, a re-evaluation was arranged. The patient reported no symptoms, without any deterioration of functional status. Also, disappearance of LBBB pattern was noted on the ECG. A myocardial perfusion scintigraphy was also carried out, at both rest and stress, without evidence of infarction or inducible ischemia. Conclusion: Acute pancreatitis can present with several ECG abnormalities, but the presence of transient LBBB in this setting is not considered very common. In fact, most of the times it seems to be correlated with electrolyte disturbances. The case presented here is regarded unique since no electrolyte abnormalities were present and a longer duration was noted. The proposed explanation and pathogenetic mechanism of this clinical manifestation is transdiaphragmatic epicardial irritation secondary to acute pancreatitis. It remains to be established by repeated assessment of the patient, whether this intermittent finding is associated with poor long-term outcome.

059: Clinical evidence of LBBB-induced cardiomyopathy: reversal by cardiac resynchronisation

Animal and clinical data have shown that left bundle branch block (LBBB) induces mechanical dyssynchrony in the left heart. In heart failure (HF) patients with low left ventricular (LV) ejection fraction, cardiac resynchronisation therapy (CRT) is much more efficient when typical LBBB is present. It has been postulated that lone LBBB could induce a progressive decline in LV function via dyssynchrony leading to chronic HF with possible recovery after CRT. However, the clinical evidence to support this hypothesis is weak. The aim of this work was to study the prevalence and characteristics of LBBB-induced cardiomyopathy cured by CRT. All the patients referred to our center for CRT implantation from 2007 to 2011 (N=375) were investigated for LBBB history. Patients were included if they presented an original syndrome consisting on: – history of typical LBBB for ≥5 years, – no evidence of structural heart disease at the time of LBBB diagnosis, – progressive development of LV systolic dysfunction and HF symptoms (NYHA class II-IV), – presence of major mechanical dyssynchrony by cardiac imaging, – absence of other etiology for cardiomyopathy, – hyper-response to CRT as indicated by LVEF>45% after 1 year. 7 patients (2% of all screened pts) had the described syndrome. The main patient characteristics and follow-up data are summarized in the following tables. Interestingly, two patients had HF symptoms and LV dysfunction recurrence after 3 and 6 years of CRT, respectively after withdraw of CRT due to device removal in one (breast cancer) and battery depletion in the other. After CRT resume, hyper-response was quickly re-observed in these two cases. These original data support the concept of LBBB-induced cardiomyopathy with possible cure by CRT. The exact prevalence of the syndrome, the time needed to develop and predictive factors need to be assessed in further prospective epidemiological studies. Table – Main characteristics. Patient characteristics at time of LBBB diagnosis Male 4 Age (years) 51 (36 to 60) Chest pain as 1 st symptom 2 Rate-dependent LBBB 3 QRS duration (msec) 136 (100 to 160) Time to HF symptoms (years) 11,5 (5 to 21) Time to CRT (years) 13,5 (16 to 22) Table – Follow up data. Pre- and post CRT Pre-implant 1 year * NYHA class I/II/III 0/3/4 5/2/0 * QRS duration (msec) 162 (150 to 180) 124 (110 to 135) * NT-pro BNP (pg/ml) 2275±3200 159±11 * LVEF (%) 30 (20 to 39) 53 (45 to 62) * LVEDD (mm) 63 (50 to 76) 50 (44 to 56) * p<0,05

Haemodynamic Benefit of Cardiac Resynchronisation Therapy Requires Left Bundle Branch Block: A Case Report

A 55-year-old woman with dilated cardiomyopathy and rate-dependent left bundle branch block had a cardiac resynchronisation therapy (CRT) device implanted. During implantation, the maximum rate of left ventricular pressure rise (dP/dtmax) was measured invasively. This case presents a description of the acute negative effect of a left bundle branch block on dP/dtmax, and the different effect of CRT on left ventricular haemodynamic function in the presence and absence of a left bundle branch block.

Rate-dependent Left Bundle Branch Block during General Anesthesia - A case report -

Department of Anesthesiology and Pain Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea Rate-dependent left bundle branch block during general anesthesia is rare, but its occurrence makes the electrocardiographic diagnosis of acute myocardial ischemia or infarction difficult. It can also be confused with slow rate ventricular tachycardia. Herein, a case of rate-dependent left bundle branch block, in a patient with no previous history of ischemic heart disease, is reported. The administration of esmolol resulted in a decrease in the heart rate, with reversion to normal sinus rhythm.

Rate-dependent left bundle branch block unmasked by adenosine

Rate-dependent left bundle branch block unmasked by adenosine

Rate-dependent Left Bundle Branch Block during Anaesthesia

Rate-dependent left bundle branch block during general anaesthesia is rare. Its occurrence makes electrocardiographic diagnosis of acute myocardial ischaemia or infarction difficult. It can also be confused with a slow rate ventricular tachycardia. We present a case of rate-dependent left bundle branch block in a patient with no previous history of ischaemic heart disease. Carotid sinus massage resulted in a decrease in heart rate and reversion to normal sinus rhythm.

El bloqueo de rama izquierda inducido por el ejercicio en pacientes con y sin enfermedad coronaria

Exercise-induced left bundle-branch block does not always denote the presence of underlying coronary artery disease. The aim of this study was to analyze the clinical characteristics and evolution of patients with rate-dependent left bundle-branch block. 9,318 consecutive exercise stress studies were reviewed. The clinical characteristics and evolution (mean follow-up: 6.9 years) of 20 patients with exercise-induced left bundle-branch block in which coronary angiography had been performed were analyzed. Eight out of 20 patients had normal coronary arteries (group A) and 12 had coronary artery disease (group B). Peak O2 consumption, peak myocardial O2 consumption, and heart rate when block appeared (132 20 vs. 95.4 23 beats/min; p = 0.002) were significantly higher in group A. Seven of the 8 patients with normal coronary arteries had chest pain coinciding with the first beat of left bundle-branch block. There were no deaths during follow-up in group A, but permanent left bundle-branch block appeared in 5 patients of this group who experienced disappearance of exercise-related pain. There were 3 deaths in group B and 2 patients had acute myocardial infarction during follow-up. One patient in each group developed atrioventricular block and required pacemaker implantation. In contrast with patients with left bundle-branch block and coronary artery disease, the prognosis of patients with painful left bundle-branch block and normal coronary arteries is good. However, the development of permanent left bundle-branch block is frequent. Atrioventricular block, although rare, may occur.

Assessment of myocardial perfusion with thallium-201 scintigraphy in exercise-induced left bundle branch block: diagnostic value and clinical significance.

Myocardial perfusion scintigraphy with thallium-201 was performed in 33 subjects (mean age 45 years, range 28-61) with exercise-induced, rate-dependent left bundle branch block (LBBB) in order to assess both the value of Thallium-201 myocardial imaging for the diagnosis of coronary artery disease (CAD) and the pathogenesis (ischaemic or not) of the conduction defect. Of the 33 patients evaluated, 16 had chest pain suggestive of CAD and 17 were asymptomatic. None had a history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 b.min-1. Eighteen patients showed repolarization abnormalities (ST segment depression with deep inverted T waves) compatible with ischaemia, after QRS normalization. Thallium-201 myocardial uptake was normal in 12 subjects; in the remaining 21, reversible Thallium-201 defects were demonstrated in the septum (18 patients), septum and apex (2), and septum and infero-apical wall (1). No patient had irreversible defects and all had normal coronary angiography, with negative ergonovine tests for coronary artery spasm. The patients were followed up for a mean of 43 months (range 16-80). One patient died from sudden death, but no cardiac event occurred in the other patients. In conclusion, exercise Thallium-201 myocardial scintigraphy showed a high prevalence (64%) of reversible perfusion defects in a group of patients with exercise-induced LBBB without any evidence of CAD at angiography or coronary spasm at ergonovine test. Moreover, follow-up showed a relatively low rate of major cardiac events.

Rate-related left bundle branch block as a cause of non-ischemic chest pain

A case is presented of rate-dependent left bundle branch block associated with chest pain in a patient with angiographically normal coronary arteries. Lactate extraction showed no evidence of myocardial ischemia. It appears that in this case, chest pain was associated with sudden ventricular asynergy rather than myocardial ischemia.

Four-year follow-up study in patients with angina pectoris and normal coronary arteriograms ("syndrome X")

In patients with typical stress-induced anginal pain, normal coronary arteries, and unimpaired left ventricular performance at rest ("syndrome X"), a reduced coronary dilatory capacity, abnormal lactate metabolism during stress, and reduction of left ventricular functional reserve have been described. A group of 40 patients with syndrome X was followed for several years to determine their long-term prognosis. In 27 patients pulmonary artery pressure and in 19 patients left ventricular ejection fraction were reassessed during rest and exercise approximately 4 years after the initial examination. In patients with stress-induced ST-segment depression, these variables did not change during the observation period. In patients with constant or rate-dependent left bundle branch block, however, there was significant deterioration of left ventricular performance during rest (pulmonary artery mean pressure, 16 +/- 3 vs. 17 +/- 4 mm Hg, p = NS; left ventricular ejection fraction, 62 +/- 5% vs. 55 +/- 5%, p less than 0.05) and exercise (pulmonary artery, 30 +/- 6 vs. 39 +/- 10 mm Hg, p less than 0.005; left ventricular ejection fraction, 59 +/- 6% vs. 49 +/- 5%, p less than 0.01). These findings suggest that in syndrome X two subgroups with distinctly different prognoses may be defined: In patients with stress-induced ST-segment depression during exercise, left ventricular performance remains well preserved; however, in patients with either constant or rate-dependent left bundle branch block, there is significant deterioration of left ventricular function within several years.

LEFT BUNDLE BRANCH BLOCK IN PREINDUCTION PERIOD OF ANESTHESIA

We has experienced a case who had normal preoperative ECG findings, however, developed a left bundle branch block (LBBB) in preinduction period of anesthesia. A 73-year-old male, with chief complaint of melena, was diagnosed as cancer of the sigmoid colon. He had no remarkable medical history nor abnormalities in preoperative laboratory findings. After entering the operating room to undergo elective resection of the sigmoid colon, lead II ECG tracing prior to mesthesia induction revealed a LBBB. However, it changed to normal sinus rhythm snddenly during our investigation of the cause. Following preoxygenation, anesthesia was induced with thiopental, intubated with succinylcholine, and maintained with nitrous oxide 66 percent in oxygen and halothane. During operation, a LBBB pattern occurred whenever heart rate increased to over 110 per minutes (rate dependent LBBB). No change in blood pressure was accompanied by these episodes.Recovery from anesthesia was uneventful. Post operative holter ECG showed intermittent LBBB with no change in GOT, GPT, CPK etc. Though LBBB itself is a relatively benign dysrhythmia, it is significant during anesthesia, because it may indicate a possible development of myocardial infarction. It is difficult to diagnose myocardial infarction on the ECG in the presence of a LBBB.

Exercise-induced left bundle branch block and its relation to coronary artery disease

The records of 2,584 consecutive patients who underwent both treadmill exercise testing and coronary cineangiography were reviewed to determine the relation between exercise-induced, acceleration-dependent left bundle branch block (LBBB) and the presence of coronary artery disease (CAD). Rate-dependent LBBB during exercise was identified in 28 patients (1.1%), who were categorized according to their presenting symptoms: classic angina pectoris, atypical chest pain, symptomatic cardiac arrhythmia and asymptomatic. Asymptomatic patients underwent a screening exercise test. CAD was present in 7 of 10 patients who presented with classic angina pectoris, but 12 of 13 patients presenting with atypical chest pain had normal coronary arteries. All 10 patients in whom LBBB developed at a heart rate of 125 beats/min or higher were free of CAD, whereas 9 of 18 patients in whom LBBB developed at a heart rate of less than 125 beats/min had CAD. Normal coronary arteries were present in 3 patients who presented with angina and in whom both chest pain and LBBB developed during exercise. It is concluded that (1) patients who present with atypical chest pain in whom rate-dependent LBBB develops on the treadmill are significantly less likely to have CAD than patients who present with classic angina; (2) the onset of LBBB at a heart rate of 125 beats/min or higher is highly correlated with the presence of normal coronary arteries, regardless of patient presentation; and (3) patients with angina in whom both chest pain and LBBB develop during exercise may have normal coronary arteries.

Chest Pain and Rate-Dependent Left Bundle Branch Block in Patients with Normal Coronary Arteriograms

A triad of exertional chest discomfort, transient rate-dependent left bundle branch block (LBBB), and normal coronary arteries is presented in seven consecutive patients. Although the clinical symptoms resembled effort angina, qualities atypical of classic angina pectoris were commonly noted: 1) the onset was always abrupt; and 2) the pain was local, never radiating; 3) palpitation; and 4) "walk through" phenomenon were often present. The abrupt pain took place simultaneously with the appearance of LBBB induced by physical exercise in all seven patients. Atrial pacing or spontaneous resting heart rate changes produced similar sensations and LBBB in four of the five patients examined in this way. Similarly, in the same four patients kinetocardiographic recordings disclosed a sudden occurrence of paradoxic cardiac movement at the moment LBBB and chest pain appeared. The paradoxic systolic motion disappeared at reversion to normal conduction.

Transient unifascicular, bifascicular and trifascicular block: Electrophysiologic correlations in a patient with rate-dependent left bundle branch block and transient right bundle branch block

Correlations of the His to ventricular (H-V) conduction time were made with the surface electrocardiogram during normal intraventricular conduction, unifascicular block (right bundle branch block), bifascicular block (left bundle branch block) and trifascicular block (right and left bundle branch block) in a patient with rate-dependent left bundle branch block who had transient right bundle branch block during recording of the His bundle electrogram. The results provide a functional confirmation of the theory that a prolonged H-V time is a manifestation of trifascicular disease.