Cardiac Resynchronization Therapy: Reconsidering Its Essence as a Treatment for Electrical Dyssynchrony in Heart Failure

Figures

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  FIGURE 1. Multifactorial model of heart failure. (A) The barrel is filled with water, and each stave represents an individual function that determines cardiac performance. The “heart failure line” is set at a certain level. (B) For example, when a new left bundle branch block develops, cardiac synchrony is impaired. This lowers the corresponding stave, causing the water level to exceed the heart failure line and leak out. The leakage represents a heart failure event. In this case, introducing cardiac resynchronization therapy (CRT) elevates the stave of synchrony, preventing further leakage and thereby stabilizing heart failure. No new heart failure events would be expected for a while, and this case is considered a CRT responder. (C) However, heart failure is a multifactorial disease. It is uncommon for all other determinants of cardiac function to remain intact when heart failure occurs due to impaired synchrony. For instance, some patients may have concomitant reductions in coronary blood flow. Although CRT can restore synchrony and stabilize heart failure, it does not improve coronary stenosis, and thus the stave for coronary blood flow remains low. During the subsequent course, heart…

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  FIGURE 2. Diagram of the relationship between electrical and mechanical dyssynchrony. CRT is not a therapy that directly acts on mechanical dyssynchrony, but rather corrects mechanical dyssynchrony through the modulation of electrical dyssynchrony. The direct target of CRT is electrical dyssynchrony. Electrical dyssynchrony represents an upstream factor contributing to worsening heart failure. Gray arrows indicate pathological pathways, whereas open arrows indicate therapeutic interventions. CRT, cardiac resynchronization therapy.

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  FIGURE 3. Flow of cardiac resynchronization therapy (CRT) in heart failure management.

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  FIGURE 4. Mechanism of interventricular septal ischemia in left bundle branch block. In left bundle branch block (LBBB), electrical conduction to the left ventricular (LV) lateral wall proceeds through the right bundle branch and detours within the myocardial layer from the apex, resulting in delayed activation and contraction of the LV lateral wall compared with the ventricular septum. This delayed contraction directs LV intracavitary pressure toward the septum and imposes significant wall stress. When this septal pressure shift occurs at end‐systole, the aortic valve remains open and LV pressure is partially relieved into the aorta. However, when it occurs in early diastole, the aortic valve is closed and the increased intracavitary pressure can impair coronary blood flow in the septal region.

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  FIGURE 5. Flowchart for CRT eligibility and recommended LV lead positioning. This flowchart summarizes an ECG‐based approach for evaluating eligibility for cardiac resynchronization therapy (CRT) and determining the recommended left ventricular (LV) lead position. Patients with QRS ≥ 120 ms are categorized according to QRS morphology, axis, and pacing status. “LBBB‐like patterns” include typical and atypical LBBB morphologies, as well as RV apical pacing patterns that resemble LBBB with left axis deviation. For eligible patients, the recommended LV lead position is indicated: LBBB, left bundle branch block; RBBB, right bundle branch block; LV A–L, left ventricular anterolateral region; LV P–L, left ventricular posterolateral region.

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  FIGURE 6. Site of maximal intraventricular conduction delay during right ventricular pacing and the effects of biventricular pacing. (A) Coronary sinus angiography was performed in an 80‐year‐old male. The anterolateral and posterolateral branches are depicted (upper panel). Electrode catheter was inserted into each branch (white circle). During RV apical stimulation (white star), Q‐LV was measured at each branch (lower panel). (B) The Q‐LV interval was longer at the anterolateral site than at the posterolateral site (left panel). Simultaneous biventricular pacing showed that the QRS duration was shorter at the anterolateral site than at the posterolateral site (middle panel). The LV dP/dt_max and LVP were higher at the anterolateral site than at the posterolateral site (right panel). The anterolateral site showed a longer Q‐LV interval, a greater QRS narrowing with simultaneous biventricular pacing, and a higher LV dP/dt_max, indicating that it is a desirable location for left ventricular lead placement. Reproduced with permission from Ogano et al. [42].

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  FIGURE 7. A case of successful cardiac resynchronization therapy for bundle branch delay. (A) A woman in her 70s. Pre‐CRT electrocardiogram showing right bundle branch block with a very small S wave in lead I (black circle), consistent with bilateral bundle‐branch delay. (B) Coronary venography demonstrated the left ventricular (LV) lateral vein (left panel). An electrode catheter was advanced to this site (middle panel), and Q‐LV measurement showed a prolonged interval of 140 ms (right panel). HRA = high right atrium. (C) The LV lead was implanted at the LV lateral wall and cardiac resynchronization therapy (CRT) was performed. Left ventricular ejection fraction improved from 34% to 45%, and the cardiothoracic ratio on chest radiograph decreased from 56% to 51%.

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  FIGURE 8. A case of successful cardiac resynchronization therapy for left anterior fascicular block. An 82‐year‐old woman with a baseline electrocardiogram showing a QRS duration of 126 ms and left anterior fascicular block. A left ventricular (LV) lead was implanted at the anterolateral site with delayed conduction, and cardiac resynchronization therapy (CRT) was initiated. After CRT, the QRS duration remained 126 ms, but the QRS axis shifted from −33° to 35°, indicating normalization. At the 6‐month follow‐up, chest radiography demonstrated improvement in the cardiothoracic ratio, and the patient's New York Heart Association (NYHA) functional class improved from III to I. Reproduced with permission from Ogano et al. [50].