left ventricular hypertrophy
Left Ventricular Hypertrophy (LVH) is an independent risk factor for sudden death in those with hypertension (a 3 fold increase) independent of the blood pressure level (Sheppard and Davies 1998; Hirsch and Adams 1993; Priori SG et al 2001)
- Hypertrophy (increased left ventricle mass)
- Concentric (increased afterload and increased sympathetic tone eg. in hypertension and activation of renin – angiotensin system)
- Eccentric (LVH with dilatation – increased preload and afterload eg. in obesity (with increased blood volume) or decompensation in a setting of atherosclerosis, valvular insufficiency, myocarditis or other cardiomyopathies).
What causes these structural changes in hypertensives (Mayat and Hughes 2003)?
- Increased pressure exerts increased load (LaPlace’s Law)
- Increased tension results in increased wall tensile stress
- Normalisation of stress achieved by either increasing wall thickness or reducing chamber diameter or both
Changes are dependent on:
- Genetic influences
- 24 hour blood pressure profile
- Arterial stiffness
- Plasma volume
- Myocardial performance
- Neurohumoral status
What are the consequences of structural changes?
- Impaired relaxation and thus a longer LV filling time, leaving more blood within the left atrium and increased atrial contraction force
- Impaired diastolic function leads to reduced LV compliance and reduced LV end diastolic volume, in turn leading to a reduction in stroke volume and symptoms of low output, such as fatigue.
- Intramyocardial blood flow is compromised, leading to myocardial fibrosis and electrical instability (myocardial fibrosis is seen in 30% of those hearts considered to be ‘abnormal’ in victims of sudden cardiac death)
- Ventricular ectopic beats, increased QT interval and VT are amongst those electrical disturbances recorded in those with LVH
significance of heart weight at autopsy
Researchers have suggested that hearts weighing >550g can reasonably be associated with an increased risk of sudden cardiac death, with the greatest risk being in those with systemic hypertension or aortic stenosis (Davies and Popple 1979).
Attempts have also been made to correlate heart weights with height and body weight, to provide some assistance to autopsy pathologists in determining ‘normal’ or ‘expected’ heart weights.
Fulton (1952) described the technique to be used to weigh ventricles individually - and thus attempt to gain an objective assessment of left and right ventricular hypertrophy - whilst values published by Hangartner et al (1985) and Kitzman et al (1988) can assist in correlating heart weight with body weight.
- Davies MJ, Popple A. Sudden unexpected cardiac death – a practical approach to the forensic problem. Histopathology. 1979; 3:255-277
- Fulton R, Hutchinson E, Morgan Jones A. Ventricular weight in cardiac hypertrophy. British Heart Journal. 1952; 14: 413-420
- Hangartner J, Marley N, Whitehead A, Thomas A, Davies M. The assessment of cardiac hypertrophy at autopsy. Histopathology. 1985; 9: 1295-1306
- Hirsch CS, Adams VI. Sudden and unexpected death from natural causes in adults. Chapter 5 in ‘Spitz and Fisher’s Medicolegal investigation of death. Guidelines for the application of pathology to crime investigation.’ Spitz WU (Ed) (3rd Ed) Charles C Thomas Publishers, Springfield Illinois, USA
- Kitzman DW, Scholz DG, Hagen PT et al. Age-related changes in normal human hearts during the first 10 decades of life. Part II (Maturity): A quantitative anatomic study of 765 specimens from subjects 20 to 99 years old. Mayo Clin Proc 1988; 63:137-146
- Mayet J, Hughes A. Cardiac and vascular pathophysiology in hypertension. Heart. 2003; 89: 1104-1109
- Priori SG, Aliot E, Blomstrom-Lundqvist C et al. Taskforce on Sudden Cardiac Death of the European Society of Cardiology. European Heart Journal. 2001; 22:1374-1450
- Sheppard M, Davies MJ. Practical Cardiovascular Pathology. 1998 Arnold Publishing, London UK