LVH is a common precursor and a strong independent risk factor for coronary heart disease (CHD), sudden cardiac death (SCD), HF and stroke. LVH in hypertensive heart disease produces structural myocardial changes including perivascular and myocardial fibrosis which precipitate diastolic dysfunction and create conditions for an arrhythmogenic substrate [3]. Although the prevalence of LVH is lower in women than in men, LVH becomes more common in post-menopausal women, and hypertension and LVH are stronger risk factors for stroke and HF in women than in men [2]. In the USA HF is associated with diastolic dysfunction in over one third of the patients with HF [3].

The traditional concept about the evolution of hypertensive heart disease postulates that LVH leads into concentric LVH and systolic HF and then progresses into diastolic HF. However, eccentric LVH is at least as common as concentric LVH according to echocardiographic data. Newer data evaluated by Drazner in his review article [4] suggest that concentric hypertrophy does not commonly progress to dilated cardiac failure after 5–7 years of follow-up in the absence of interval myocardial infarction and that LVH in hypertensive patients can evolve directly to dilated HF rather than first evolving into concentric hypertrophy.

The block diagram in Fig. 7.1 is a schematic of the pathway of the evolution of LVH into left ventricular dysfunction and HF. The bottom section of the diagram lists ECG findings that can be expected in the course of the evolution. When early signs of diastolic dysfunction develop and the ejection fraction (EF) is still within normal limits, various ECG abnormalities that can be expected include transient AF, old ECG-MI, ECG signs of left atrial overload, wide QRS/T angle, delayed epicardial repolarization time (RTepi) and prolonged rate-adjusted QTend (QTea).

Frequently used ECG-LVH criteria in prognostic evaluation are listed in Table 7.1 as common reference for this chapter. The following criteria were included: Sokolow-Lyon [5], Minnesota Code [6], Cornell voltage [7], Cornell product [8], Estes score [9] and Perugia score [10].

Several ECG models have been introduced for prediction of left ventricular mass (LVM) on a continuous scale (Echo-LVM) [11–13] including a model derived in the Cardiovascular Heart Study (CHS) [13]. The algorithms for LVM from the CHS model are listed in Table 7.2 for normal ventricular conduction, anterior/lateral MI and ventricular conduction defects according to the Minnesota Code. Ranking of the best individual variables in each model according to their partial R-square values revealed that body weight was a dominant predictor in normal conduction, inferior myocardial infarction (MI) and right bundle branch block (RBBB), QRS duration in left bundle branch block (LBBB) and anterior and lateral MI and JV6 amplitude in indetermined-type ventricular conduction defect (ICVD) (not shown). The correlation between ECG-LVM from this model and Echo-LVM was 0.54 in women and 0.51 in men. In CHS study ECG-LVM and Echo-LVM had about equally strong associations with overt and subclinical disease and with risk factors for left ventricular hypertrophy.