Pathological causes of LVH

My last article looked at the assessment of Left Ventricular Hypertrophy; its contextual clinical significance and subsequent electrocardiographic findings, and concluded with possible pathological reasons for the development of LVH of which I wanted to discuss in my next article.

Sadly, due to an onslaught of assignments more intimidating than Xerxes Persian army in the film 300, I haven’t had the time to write any subsequent material.

However, now the assignments are over I have the time to explore these pathological causes of LVH.

Just as a recap, LVH is an increase in the size and proportion of the left ventricular myocardium. Just like any muscle, the more it is permitted to carry out work (contract) the greater it will increase in size (hypertrophy).

This increase in muscular size results from increased recruitment of sarcomeres (basic subunit of muscle cells) as well as extra cellular matrix remodeling (the scaffolding material of tissue). As a result of these anatomical adaptations the ventricle changes in size and proportion. Its normal conoid shape may be altered.

Concentric/Eccentric Hypertrophy

This remodeling will present as either Concentric or Eccentric hypertrophy depending on the underlying cause.

Concentric hypertrophy results from chronic pressure overload commonly associated with chronic hypertension and aortic stenosis. New sarcomeres are added in parallel to existing sarcomeres. Wall thickness greatly increases and persistence over time will significantly reduce chamber radius. The remodeled ventricle has reduced contractility  and compliance leading to diastolic and eventually systolic dysfunction (impaired filling/ejection).

Eccentric hypertrophy often occurs with volume and pressure overload; pathological associations include heart failure; aortic/mitral regurgitation (volume overload) and chronic hypertension (pressure overload). Ventricular remodeling results in increased chamber radius and moderate increases in wall thickness. Chamber dilation occurs as new sarcomeres are added in series to existing sarcomeres.



Physiological consequences of LVH

LVH usually develops as a compensatory response to the underlying pathologies mentioned above. Increased arterial pressure (afterload) as a result of chronic hypertension and/or aortic stenosis increases the pressure required of the LV to eject this blood.  Increased LV wall tension compensates via concentric hypertrophy.

Volume overload within the heart (heart failure) is often a resultant of valvular regurgitation and/or systolic dysfunction. Aortic/mitral regurgitation will increase the volume of blood left in the ventricle after systole (End Systolic Volume). During the next systolic cycle the LV has to contract with greater force to eject this increased volume of blood (End Diastolic Volume). Frank Starlings law of the heart states that increased stretch on the myocardial wall (Preload) increases strength of contraction. This pressure/volume overload induces chamber dilation and eccentric hypertrophy.

The hypertrophied LV becomes less compliant reducing its filling and contractile capacities. This culminates in systolic dysfunction. Systolic dysfunction is a significant reduction in cardiac output and will present with symptoms of dizziness, fatigue and shortness of breath. Systolic dysfunction of the LV will also lead to pulmonary congestion due to the back up of pressure generated by increased atrial and pulmonary venous pressures resulting from the increased EDV.

LVH is one of the strongest predictors of cardiac morbidity in hypertensive patients. The degree of hypertrophy correlates with the development of congestive heart failure, angina, arrhythmia, myocardial infarction and cardiac death (Lilly).

Another pathological subcategory I have not eluded to that is also a major contributor to LVH is cardiomyopathies. This is something I will look at in detail in my next article. Thanks for reading 🙂



I’d just like to take the opportunity to thank my good friend and partner in crime Christopher Wild for firstly creating this fantastic physiology based resource and secondly giving me the opportunity to participate in its progression.

3 months since creation and the TSP has already received nearly 1500 hits, recognition and support from numerous universities and academics across the country as well as our professional governing body.

My buddy deserves massive acclamation for this achievement and I know there is much more to come!

Whilst writing this article it has again reminded me how interconnected many pathologies, symptoms and clinical findings can be. About half way through writing I felt as though I’d opened a big can of worms as there are so many different tangents on which you could proceed to discuss. Added to this is the limited knowledge I have as I’m only a second year student! Therefore please don’t take this information as cardiology gospel! I have and always will, use reliable sources of information, but this is my interpretation of such material and I can’t guarantee inclusion of every detail.  Nevertheless, I have personally found writing such articles to be of great benefit; and thus if there are any other physiology students out there that may be interested in writing for TSP we would greatly welcome your support.

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Lilly, L. S. (ed.) (2010) Pathophysiology of heart disease: A collaborative project of medical students and faculty. Editor, Leonard S. Lilly. 5th edn. Philadelphia, PA: Lippincott Williams and Wilkins.
(Lilly, 2010, pp. 315 – 315)

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Student healthcare Scientist (Cardiac Physiologist) @ UWE

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