Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. DCM is generally caused by viral/bacterial myocarditis, exposure to cardiotoxic substances or is a manifestation of a systemic disease. Before cell death and fibrotic repair occur, multiple factors contribute to contractile dysfunction, including abnormalities in sarcolemmal integrity, energy production, calcium handling and force transmission. 10 Both systolic and diastolic dysfunction worsen with time and EF is progressively reduced, with symptoms and signs of HF. Secondary LVHCardiomyocyte hypertrophy is the primary mechanism by which the heart counteracts a protracted increase in stress (or load) on the ventricular wall. 11 According to Laplace's law, 12 wall stress is directly related to LV cavity size and intracavitary pressure and inversely related to wall thickness. Thus, wall thickening will counteract, at least in part, the increased stress and oxygen demand caused by pressure or volume overload, although, in the long run, this compensatory mechanism may become maladaptive. On the other hand, several other nonhemodynamic factors, including activation of the adrenergic and renin-angiotensin-aldosterone (RAAS) systems, release of growth factors and cytokines, contribute to the development of LVH. 13,14 Pressure Overload In most cases, pressure overload manifests as arterial hypertension (AH) or aortic stenosis (AS).Hypertensive Heart The most common condition associated with an increase in cardiac afterload and wall stress is AH. 15 Approximately 20-60% of patients with uncomplicated AH have evidence of increased LVM on echocardiography. 16 LVM can increase from wall thickening, chamber dilatation or both. Wall thickening occurs more commonly in response to pressure overload whereas chamber dilation occurs more commonly in response to volume overload. Although LV wall thickness is more closely related to systemic diastolic blood pressure (concentric hypertrophy), reflecting pure pressure load caused by increased systemic vascular resistance...

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Left ventricular noncompaction (LVNC) is an increasingly recognised cardiomyopathy characterised by excessive trabeculation and deep intertrabecular recesses in direct communication with the left ventricular cavity. In LVNC, hypertrabeculation has been associated with heart failure, ventricular arrhythmia, and systemic thromboembolism. However, hypertrabeculation alone is not sufficient to define a subject as at risk for such complications and thus should not be sufficient to diagnose LVNC. Despite several studies having investigated parameters to predict adverse cardiovascular events, physicians have no effective tools to differentiate between clinically silent hypertrabeculation and LVNC. The aim of this paper was to review literature on LVNC diagnostic criteria and to provide an easy and accessible diagnostic algorithm to distinguish between hypertrabeculation phenotype, non-compaction phenotype and LVNC cardiomyopathy.