Most patients with mild or moderate LVH have no symptoms. However, if the LVH is severe there may present with:

• Arrhythmias
• Dyspnea
• Orthopnea
• Chest pain
• Murmur
• Severe hypertension
• Pedal edema
• Dizziness
• Syncope

The symptoms usually occur after chronic LVH has developed. In many cases, the symptoms may be of the primary disorder that has caused the LVH.

The diagnosis of LVH is usually initially based on the ECG and the following criteria have been established.

Cornell product:

• S in V3 and R in aVL >24 mm (men) and 20 mm (women)

Sokolow Lyon voltage:

• S in V1 and R in V5 or V6 = or > 35 mm
• R in AVL = or > to 11 mm

There may be repolarization changes such as QRS prolongation, left axis deviation and left ventricular strain and left atrial enlargement. LVH based on ECG is often underdiagnosed in patients with obesity, pectus deformity and chronic obstructive pulmonary disease (COPD). It is important to note that there is very poor correlation between ECG and left ventricular mass. However ECG is inexpensive, accessible and is ideal for high risk patients with ischemic heart disease and hypertension. The technique can also assess for presence of Q waves, arrhythmias, and left bundle branch block.

Echocardiography is the procedure of choice to asses left ventricular mass. In addition the technique can also assess for systolic and diastolic dysfunction, left atrial size, function of valves, presence of blood clots and ejection fraction.

The gold standard test to examine left ventricle mass is the cardiac MRI [8]. It does not require any contrast and does not use radiation. The technique can also assess left atrium size, function of valves and ventricular function and it can determine other causes of left ventricular hypertrophy and provide prognostic information [9] [10]. Downside of cardiac MRI is expense and lack of availability.

In general the following patients should have an echocardiography or cardiac MRI:

• Symptomatic patients
• Signs of CHF
• Presence of hypertension
• Concern for congenital hypertrophic cardiomyopathy
• Presence of other risk factors for LVH
• ECG evidence of LVH

Once LVH has been diagnosed, the primary condition that is causing it needs to be treated. Many studies have shown that regression of LVH can occur but this can take several months or even years. For people with hypertension, many types of antihypertensive are used to treat the disorder [11]. But when it comes to LV mass regression, the drugs of choice are calcium channel blockers or ACE inhibitors. Several studies have shown the use of ACE Inhibitors can result in improvement in diastolic function after a year. However, the reduction in stroke risk just based on LV mass reduction is not clear cut. Many of these patients have other risk factors like diabetes mellitus, hyperlipidemia, smoking and obesity. There is insufficient data to recommend treatment only for the reduction of LV mass a treatment goal.

• In patients with diabetes mellitus with LVH, some studies have shown that the lowering of blood pressure can result in regression of LVH and may even reduce the incidence of new onset atrial fibrillation.
• In addition, patients should have a low salt diet and undergo weight loss if obese. This can further help reversing LVH.
• Majority of patients with chronic hypertension will need more than one anti-hypertensive medication. It is important for healthcare providers to understand that lowering the blood pressure to a selected target is far more important than selecting the type of antihypertensive agent.
• The clinician should select antihypertensives based on presence or absence of other comorbidities, their effectiveness and adverse effects.
• The drugs of choice to reverse LVH include ACE inhibitors and calcium channel blockers.
• Beta blockers may be useful in patients with coronary artery disease, angina pectoris and in individuals with other comorbid conditions like portal hypertension, atrial fibrillation, thyrotoxicosis, esophageal varices and benign essential tremor. in addition, patients with systolic dysfunction or CHF may benefit from beta blockers like bisoprolol, carvediol or metoprolol.

If the left ventricular hypertrophy is treated, it can be reversed in most cases leading to a decrease in morbidity. However, if the LVH is not treated it can result in several complications including the following:

• Congestive heart failure in the presence of normal systolic function
• Congestive heart failure in the presence of impaired systolic function
• Diastolic dysfunction is more common in elderly females with normal ejection fraction and presence of heart failure
• Atrial arrhythmias
• Ventricular arrhythmias [7]
• Sudden cardiac death
• Coronary artery disease with myocardial infarction
• Stroke

There are no long term studies indicating that reversing LVH also leads to improved survival or decreased risk of heart disease. The reason for this is that there are other risk factors for heart disease and stroke that also need to be treated at the same time. Just treating LVH alone for decreasing morbidity is not recommended clinical practice.

There are many causes of LVH which include the following:

• Hypertension is the most common. Patients with chronic untreated hypertension may have severe LVH but treatment can reverse the condition.
• Diabetics are also known to develop LVH in the absence of hypertension or coronary artery disease.
• Obese individuals also develop LVH but the exact cause is not known. Some studies indicate that a combination of weight, hypertension or sleep apnea may be contributing factors.
• Older people generally tend to have LVH, but it mild in nature.
• Obstructive sleep apnea patients are known to have LVH. If left untreated it can lead to congestive heart failure (CHF), myocardial infarction (MI), cerebrovascular accident (CVA), arrhythmias, pulmonary hypertension and hypertension. There continues to be debate on obstructive sleep apnea and LVH. There is a belief that the cause of LVH may not be directly related to sleep apnea but to the existing hypertension
• Aortic stenosis is the most common valvular heart disorder causing LVH [5].
• Aortic regurgitation
• Athletes usually have varying degrees of LVH.
• Congenital hypertrophic cardiomyopathy
• Amyloidosis
• Sarcoidosis
• Chronic renal failure [6]

There are no solid data on prevalence of LVH. There is no study that has reported LVH incidence based solely on ECG or echocardiogram. However, the conditions that cause LVH like hypertension, aortic stenosis or diabetes mellitus are very common and it is assumed that LVH is also a frequent occurrence. Since LVH always occurs in association with other traditional cardiac risk factors, it is usually mentioned. The chief reason is that the ECG is not very sensitive for detecting LVH and echocardiogram is not normally used to screen patients with LVH. LVH has been reported in both genders and in people of all ages. No race is immune from development of LVH. The exact number of hypertensive and diabetics patients who have LVH has never been reported but the numbers are not miniscule. Autopsy data show that LVH is a frequent finding in patients with aortic stenosis and hypertension.

When the left ventricle encounters increased afterload or elevated systolic or diastolic pressure, it adapts by increasing its muscle mass. Histological studies reveal that there is an increase in the size of myofibrils and fibrosis. If the increased pressure or volume overload is not reversed, then the increased hypertrophy continues resulting in abnormalities of the intramyocardial coronary vessels. Histological studies showed that in patients with severe left ventricular hypertrophy there is medial hypertrophy with perivascular fibrosis. In addition, the mechanical stress on the left ventricular wall from the increased pressure results in generation of growth factors, neurohormones and cytokines like insulin and angiotensin ll. LVH is most common with pressure overload and the hypertrophy is more concentric. When the left ventricle is faced with an increased volume overload as in aortic or mitral regurgitations, the hypertrophy is more eccentric.

Based on existing data it is suggested that patients with hypertension have a yearly ECG to look for LVH as part of standard evaluation. This should be followed by an echocardiogram. However the role of echocardiography as a screening tool for LVH is not established. Only patients with other risk factors for heart disease and those with symptoms should undergo echocardiography. Nonetheless some experts indicate that the low cost examination may be cost effective, especially if it can lead to a decrease in risk of heart disease. Since LVH is a marker for severe disease, its presence should suggest more aggressive management by the healthcare provider. Further, these patients will need serial ECGs and echocardiograms to determine if the LVH is decreasing after treatment. Since the most common cause of LVH is hypertension, it is imperative that the condition be adequately treated. Measurement of blood pressure regularly is a key to preventing LVH.

To prevent worsening of LVH, patient should be asked to reduce salt intake and control body weight. Most patients with hypertension and LVH may require more than one antihypertensive agent. However, clinicians should remember that reaching the target blood pressure is more important that the type of agent used. While beta blockers do not induce regression of LVH they do have a role in the treatment of hypertension. The beta blockers may have a role in management of patients with angina pectoris, atrial fibrillation for rate control, and in patients with systolic dysfunction with heart failure (carvediol, bisoprolol, metoprolol). At the same time, it is vital to treat risk factors for ischemic heart disease like diabetes mellitus, discontinuation of smoking, encourage exercise and lower levels of lipids.

Left ventricular hypertrophy (LVH) is essentially an increase in left ventricular mass and is also a form of myocardial remodeling. Left ventricular hypertrophy is considered to be a normal adaptive mechanism caused by an increased workload of the heart, of which the most common cause is hypertension [1]. However, there are many other causes of LVH including aortic stenosis, coarctation of aorta, thyrotoxicosis, obstructive sleep apnea and diabetes mellitus [2]. In the short term, an increase in left ventricular mass may be of some benefit to the individual as it permits the myocardium to compensate for any increase in wall stress. The adaptation can also help overcome any acute hemodynamic compromise. However, in the long run, left ventricular hypertrophy is harmful. Chronic LVH has been recognized as a risk factor for cardiovascular events, stoke and premature death [3]. When it comes to diagnosis, one needs to be aware that the ECG is relatively insensitive for detecting prognostically significant LVH [4].

Despite extensive data linking ECG and echocardiographic evidence of ventricular hypertrophy to a higher risk of cardiovascular disease, LVH alone is not thought to be as a classic or standard risk factor for heart disease. The other reason is that left ventricular mass is often difficult to quantify with transthoracic echocardiogram. In addition, there are only sparse data showing that reversing LVH improves outcomes. On the other hand, there is ample medical literature showing that lowering of blood cholesterol, blood pressure, discontinuation of tobacco and exercise have important clinical benefits. Finally, although echocardiography is more sensitive than ECG in detecting left ventricular mass, its routine use in patients with hypertension is still being debated.

Even mild cases of hypertension are associated with an increase in left ventricular mass. The important thing is that the left ventricular hypertrophy associated with hypertension is reversible and longtime blood pressure therapy does have benefits. Data show that use of angiotensin converting enzyme (ACE) inhibitors or calcium channel blockers are more effective at reducing left ventricular mass than other antihypertensive drugs.

Left ventricular hypertrophy (LVH) is basically an increase in the size of the left ventricle. The most common cause of LVH is high blood pressure, especially when it is not treated. Other causes of LVH include diabetes mellitus, aortic valve disease, narrowing of the aorta and systemic disorders like hyperactive thyroid gland. Most patients have no symptoms initially but if the LVH is untreated, it can present with heart failure, stroke or a heart attack. The diagnosis of LVH is initially made by an ECG and can be confirmed by an echocardiogram. The treatment of LVH requires treating the condition causing it and in most cases this means treating the high blood pressure. If treated, the LVH can reverse and this decreases the risk of stroke and heart disease.

1. Woodiwiss AJ, Norton GR. Obesity and left ventricular hypertrophy: the hypertension connection. Curr Hypertens Rep. 2015 Apr;17(4):539.
2. Hensley N, Dietrich J, Nyhan D, Mitter N, Yee MS, Brady M. hypertrophic cardiomyopathy: a review. Anesth Analg. 2015 Mar;120(3):554-69.
3. Shenasa M, Shenasa H, El-Sherif N. Left Ventricular Hypertrophy and Arrhythmogenesis. Card Electrophysiol Clin. 2015 Jun;7(2):207-220. 
4. Palmiero P, Zito A, Maiello M, Cameli M, Modesti PA, Muiesan ML, Novo S, Saba PS, Scicchitano P, Pedrinelli R, Ciccone MM. Left ventricular diastolic function in hypertension: methodological considerations and clinical implications. J Clin Med Res. 2015 Mar;7(3):137-44
5. Rader F, Sachdev E, Arsanjani R, Siegel RJ. Left ventricular hypertrophy in valvular aortic stenosis: mechanisms and clinical implications. Am J Med. 2015 Apr;128(4):344-52.
6. Leibowitz D. Left ventricular hypertrophy and chronic renal insufficiency in the elderly. Cardiorenal Med. 2014 Dec;4(3-4):168-75
7. Chatterjee S, Bavishi C, Sardar P, Agarwal V, Krishnamoorthy P, Grodzicki T, Messerli FH. Meta-analysis of left ventricular hypertrophy and sustained arrhythmias. Am J Cardiol. 2014 Oct 1;114(7):1049-52.
8. Bacharova L, Ugander M. Left ventricular hypertrophy: The relationship between the electrocardiogram and cardiovascular magnetic resonance imaging. Ann Noninvasive Electrocardiol. 2014 Nov;19(6):524-33. 
9. Călin A, Roşca M, Beladan CC, Enache R, Mateescu AD, Ginghină C, Popescu BA. The left ventricle in aortic stenosis--imaging assessment and clinical implications. Cardiovasc Ultrasound. 2015 Apr 29;13:22
10. Fattal J, Henry MA, Ou S, Bradette S, Papas K, Marcotte F, Garceau P, Pressacco J. magnetic resonance imaging of hypertrophic cardiomyopathy: beyond left ventricular wall thickness. Can Assoc Radiol J. 2015 Feb;66(1):71-8
11. Charytan D. Is left ventricular hypertrophy a modifiable risk factor in end-stage renal disease. Curr Opin Nephrol Hypertens. 2014 Nov;23(6):578-85.