Diffuse Myocardial Fibrosis Reduces Electrocardiographic Voltage Measures of Left Ventricular Hypertrophy Independent of Left Ventricular Mass

Abstract

BackgroundMyocardial fibrosis quantified by myocardial extracellular volume fraction (ECV) and left ventricular mass (LVM) index (LVMI) measured by cardiovascular magnetic resonance might represent independent and opposing contributors to ECG voltage measures of left ventricular hypertrophy (LVH). Diffuse myocardial fibrosis can occur in LVH and interfere with ECG voltage measures. This phenomenon could explain the decreased sensitivity of LVH detectable by ECG, a fundamental diagnostic tool in cardiology.Methods and ResultsWe identified 77 patients (median age, 53 [interquartile range, 26–60] years; 49% female) referred for contrast‐enhanced cardiovascular magnetic resonance with ECV measures and 12‐lead ECG. Exclusion criteria included clinical confounders that might influence ECG measures of LVH. We evaluated ECG voltage‐based LVH measures, including Sokolow‐Lyon index, Cornell voltage, 12‐lead voltage, and the vectorcardiogram spatial QRS voltage, with respect to LVMI and ECV. ECV and LVMI were not correlated (R 2=0.02; P=0.25). For all voltage‐related parameters, higher LVMI resulted in greater voltage (r=0.33–0.49; P<0.05 for all), whereas increased ECV resulted in lower voltage (r=−0.32 to −0.57; P<0.05 for all). When accounting for body fat, LV end‐diastolic volume, and mass‐to‐volume ratio, both LVMI (β=0.58, P=0.03) and ECV (β=−0.46, P<0.001) were independent predictors of QRS voltage (multivariate adjusted R 2=0.39; P<0.001).ConclusionsMyocardial mass and diffuse myocardial fibrosis have independent and opposing effects upon ECG voltage measures of LVH. Diffuse myocardial fibrosis quantified by ECV can obscure the ECG manifestations of increased LVM. This provides mechanistic insight, which can explain the limited sensitivity of the ECG for detecting increased LVM.

Association of ECG parameters with late gadolinium enhancement and outcome in patients with clinical suspicion of acute or subacute myocarditis referred for CMR imaging

“…Underlying structural abnormalities such as fibrosis and oedema impact electrical homogeneity across the heart leading to conduction delays, resulting in abnormal ECG findings. These are not isolated to significant transmural enhancement, but other patterns such as diffuse fibrosis in left ventricular hypertrophy [23]. Specifically for myocarditis, it was demonstrated in 65 patients with biopsy-proven myocarditis that 77% had an abnormal ECG, similar to our findings that 78% of the population had an abnormal ECG, and this was associated with LGE findings where bundle branch block was observed with septal enhancement, ST-abnormalities with lateral enhancement, while transmural LGE in the lateral wall was associated with Q-waves [24].…”

IFITM3 protects the heart during influenza virus infection

“…IFITM3 Protects Mice from Excess Collagen Deposition in the Heart during Infection. Cardiac fibrosis results from excess fibroblast secretion of extracellular matrix components, particularly collagen, and unresolved collagen accumulation has been shown to reduce the efficiency of electrical conductivity of the heart (40,41). Thus, we hypothesized that fibrotic collagen deposition may be linked to the severe cardiac electrical defects observed in PR8-infected IFITM3 KO mice.…”

N-Terminal Propeptide of Collagen Type Iii as a Proposed Marker of Myocardial Fibrosis in Type 2 Diabetes

“…Согласно полученным данным, у пациентов из группы с СД-2 оказались значительно выше размеры миокарда левого желудочка. В то же время, эти изменения сочетаются с падением вольтажа ЭКГ у пациентов с СД-2, что, согласно некоторым исследованием, характерно именно для фиброза миокарда, в отличие от истинной мышечной гипертрофии миокарда, когда вольтаж ЭКГ, напротив, должен бы расти [8,9]. Для подтверждения предположений о том, что вышеуказанные изменения связаны именно с фиброзом миокарда, пациентам был исследован PIIINP.…”

“…Есть работы, доказывающие, что помощь в диагностике фиброза миокарда может оказать банальный анализ стандартных эхокардиографических и электрокардиографических (ЭКГ) показателей. Известно, что при фибротическом поражении серд ца одновременно с увеличением массы миокарда левого желудочка падает вольтаж ЭКГ [8,9], в то время как при истинной мышечной гипертрофии он должен был бы увеличиваться. Однако такие нестандартные методы диагностики фиброза миокарда хоть и являются перспективными, но в то же время довольно косвенными.…”