Left ventricular hypertrophy

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Classification according to ICD-10
I51.7 Cardiomegaly, ventricular dilation
ICD-10 online (WHO version 2019)
Graphic representation of left ventricular hypertrophy in a short axis section.

As left ventricular hypertrophy (LVH) and left ventricular hypertrophy called, refers to the tissue enlargement ( hypertrophy ), which the heart muscle (myocardium) of the left ventricle concerns (ventricles). LVH is a special form of cardiomegaly (abnormal enlargement of the heart).

Epidemiology

About 20 to 60% of patients with chronic high blood pressure have left ventricular hypertrophy.

pathology

The ECG of a patient with left ventricular hypertrophy with an increased Sokolow-Lyon index, reduced ST segment and negative T waves in the left ECG leads .
Echocardiographs of the parasternal long axis: Clearly visible left ventricular hypertrophy with increased septal thickness.

Left ventricular hypertrophy is an adaptation mechanism (adaptation) of the heart to an increased chronic stress on the heart muscle of the left ventricle. This increased stress can be triggered by both hemodynamic and non-hemodynamic processes. For example, arterial hypertension (high blood pressure), a heart valve defect , hypertrophic cardiomyopathy , but also (rare) storage diseases (e.g. Fabry's disease ) can cause left heart hypertrophy . The heart muscle mass increases as a result of the increased stress. The main difference to a sports heart , a non-pathological cardiomegaly, is that the diastolic and systolic functions are changed by a hypertrophy of the connective and adipose tissue between the muscle tissue. In addition, the macro- and microvascular blood circulation is disturbed.

Even in healthy people, the mass of the heart increases proportionally to age. This increase in mass is essentially caused by the increase in the wall thickness of the left heart ventricle. The reason for this is a loss of elasticity of the heart muscle and arterial blood vessels that goes along with age, which increases blood pressure at rest and especially during physical exertion.

In addition to the direct correlation to systolic blood pressure, other factors such as age, gender, ethnicity, body mass index , stimulation of the renin-angiotensin-aldosterone system and the sympathetic nervous system also play an important role in the pathogenesis .

The increased pressure load on the heart initially leads to an increase in muscle fiber thickness. The muscle fiber length and the chamber volume do not change. The hypertrophy of the heart muscle is concentric . If the pressure load is so high that the muscle's force of contraction is no longer sufficient, then after the systole (the ejection phase of the heart during which the heart contracts), more blood remains in the chamber, the end-diastolic volume increases and structural dilation (rearrangement in the Structure of the heart muscles) develops.

Clinical relevance

In addition to age, left ventricular hypertrophy is the most important predictor of cardiovascular disease in hypertensive patients. It is an independent risk factor for coronary artery disease , sudden cardiac death , heart failure and stroke and thus for cardiovascular morbidity and mortality as a whole.

diagnosis

In the electrocardiogram, left ventricular hypertrophy shows an increased Sokolow-Lyon index above 3.5 mV and a Lewis index above 1.6 mV. Left ventricular hypertrophy can be made visible using imaging methods such as echocardiography (ultrasound examination of the heart) or cardiac magnetic resonance imaging (MRT).

treatment

Depending on the cause of LVH, this type of cardiomegaly can be temporary. Reducing blood pressure can cause tissue enlargement to regress. The ideal treatment for left ventricular hypertrophy does not yet exist. Usually beta blockers and calcium antagonists such as verapamil are prescribed. They improve diastolic filling and coronary blood flow without further stimulating hypertrophy. ACE inhibitors reduce blood pressure and increase the heart's output.

Medical history

The British doctor and "father of nephrology" Richard Bright (1789–1858) was the first to recognize the connection between left ventricular hypertrophy and dilation of the aorta in patients with terminal kidney failure in 1827 . In 1933, Alfred Chanutin and Edwin E. Barksdale from the University of Virginia found experimentally that the diameter of the left ventricular muscle fibers increases with increasing arterial blood pressure.

further reading

Individual evidence

  1. ↑ IW Hammond, RB Devereux et al. a .: The prevalence and correlates of echocardiographic left ventricular hypertrophy among employed patients with uncomplicated hypertension. In: Journal of the American College of Cardiology . Volume 7, Number 3, March 1986, pp. 639-650, ISSN  0735-1097 . PMID 2936789 .
  2. ↑ DD Savage, JI Drayer et al. a .: Echocardiographic assessment of cardiac anatomy and function in hypertensive subjects. In: Circulation . Volume 59, Number 4, April 1979, pp. 623-632, ISSN  0009-7322 . PMID 421302 .
  3. ↑ a b C. Winneguth: Comparative study of the ACE inhibitors ramipril and captopril on their influence on the regression of left ventricular hypertrophy and on the behavior of ventricular arrhythmias. Dissertation, FU Berlin, 2006
  4. ↑ B. Eber: Left ventricular hypertrophy and arterial hypertension in everyday practice - The LIIFE-in-LIFE project. In: J Hyperton. Volume 12, Number 2, 2008, pp. 12-16.
  5. ↑ EG Lakatta, FC Yin: Myocardial aging: functional alterations and related cellular mechanisms. In: American Journal of Physiology-Heart and Circulatory Physiology . 1982; 242: H927-H941, PMID 6283905 . (Review).
  6. ↑ a b K. H. Tragl: Handbook of internal geriatrics. Verlag Springer, 1999, ISBN 3-211-83227-0 , pp. 40-42. limited preview in Google Book search
  7. ↑ a b A. H. Gradman, F. Alfayoumi: From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease. In: Progress in cardiovascular diseases. Volume 48, Number 5, 2006, pp. 326-341, ISSN  0033-0620 . doi : 10.1016 / j.pcad.2006.02.001 . PMID 16627048 . (Review).
  8. ↑ E. Agabiti-Rosei, ML Muiesan: Left ventricular hypertrophy and heart failure in women. In: Journal of hypertension. Supplement: official journal of the International Society of Hypertension. Volume 20, Number 2, May 2002, pp. S34-S38, ISSN  0952-1178 . PMID 12183849 . (Review).
  9. ↑ Prof. FC Luft, Berlin, honored: journey of discovery in the renin-angiotensin system. ( Memento of the original from November 7, 2007 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. In: heart. 30, 2005, p. 343. @1@ 2Template: Webachiv / IABot / www.bnk.de
  10. ^ R. Bright: Reports of Medical Cases, Selected with a View of Illustrating the Symptoms and Cure of Diseases by a Reference to Morbid Anatomy. Volume 1, Longmans, 1827-1831.
  11. ^ R. Bright: Cases and observations, illustrative of renal disease accompanied with the secretion of albuminous urine. In: Guy's Hospital Reports. 1836, pp. 338-379.
  12. ↑ K. Tyralla, K. Amann: Morphology of the heart and arteries in renal failure. In: Kidney International . Number 84, May 2003, pp. S80-S83, ISSN  0098-6577 . PMID 12694316 . (Review).
  13. ↑ A. Chanutin and EE Barksdale: Experimental renal insufficiency produced by partial nephrectomy. In: Arch Intern Med . Volume 52, 1933, pp. 739-751.
  14. ↑ S. Grünig: Comparison between physiological versus pathological left ventricular hypertrophy - a study on three mouse models. Dissertation, Julius-Maximilians-Universität Würzburg, 2009, pp. 9-10.