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

M D Bogaard1, G E Leenders, P A Doevendans

  • 1Department of Cardiology, University Medical Center Utrecht, Heidelberglaan 100, Q05.2.314, 3584 CX Utrecht, the Netherlands.

Insights

Cardiac resynchronisation therapy (CRT) improved left ventricular function in a patient with dilated cardiomyopathy. CRT mitigated the negative impact of left bundle branch block on pressure rise, enhancing cardiac performance.

Area of Science:

  • Cardiology
  • Biomedical Engineering
  • Cardiac Electrophysiology

Background:

  • Dilated cardiomyopathy (DCM) often presents with conduction abnormalities like left bundle branch block (LBBB).
  • LBBB can impair left ventricular (LV) systolic function and worsen heart failure symptoms.
  • Cardiac resynchronisation therapy (CRT) is a treatment option for eligible heart failure patients.

Purpose of the Study:

  • To describe the acute hemodynamic effects of LBBB on LV pressure dynamics.
  • To evaluate the impact of CRT on LV function in the presence and absence of LBBB.
  • To analyze the invasively measured maximum rate of left ventricular pressure rise (dP/dt(max)) as a functional parameter.

Main Methods:

  • Invasive hemodynamic monitoring during CRT implantation.
  • Measurement of LV pressure and its first derivative (dP/dt) to assess contractility.
  • Comparison of dP/dt(max) before and after CRT, with and without LBBB.

Main Results:

  • A significant acute negative effect of LBBB on dP/dt(max) was observed.
  • CRT demonstrated a differential effect on LV hemodynamics depending on LBBB presence.
  • CRT improved dP/dt(max), indicating enhanced LV contractility and function.

Conclusions:

  • LBBB acutely impairs LV systolic performance, as evidenced by reduced dP/dt(max).
  • CRT can effectively improve LV hemodynamic function in patients with DCM and LBBB.
  • Invasive dP/dt(max) measurement is a valuable tool for assessing CRT response.

Related Concept Videos

Dysrhythmias IV: Characteristics of Bradyarrhythmias01:18

Dysrhythmias IV: Characteristics of Bradyarrhythmias

Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Dysrhythmias VI: Management of Dysrhythmias01:25

Dysrhythmias VI: Management of Dysrhythmias

Dysrhythmia management involves a multifaceted approach, incorporating pharmacological treatments, medical procedures, surgical interventions, lifestyle modifications, and patient education.Pharmacological ManagementAntiarrhythmic Drugs:Class I (Sodium Channel Blockers): This class includes quinidine and procainamide, which reduce the speed of impulse conduction in the heart, stabilize the cardiac membrane, and control arrhythmias. Quinidine and procainamide are Class IA agents that prolong the...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...