eMedicine Specialties > Cardiology > Atherosclerosis and Risk Factors

Hypertensive Heart Disease: Differential Diagnoses & Workup

Author: Kamran Riaz, MD, Clinical Assistant Professor, Department of Internal Medicine, Section of Cardiology, Wright State University School of Medicine
Coauthor(s): Aqeel Ahmed, MD, Staff Physician, Department of Pathology, University of Missouri at Kansas City
Contributor Information and Disclosures

Updated: Aug 31, 2009

Differential Diagnoses

Coronary Artery Atherosclerosis

Other Problems to Be Considered

Hypertrophic cardiomyopathy
Athlete's heart (with LVH)
Congestive heart failure due to other etiologies
Atrial fibrillation due to other etiologies
Diastolic dysfunction due to other etiologies
Sleep apnea

Workup

Laboratory Studies

  • Recommendations from JNC 7 include the following baseline laboratory work-up before initiating the treatment for hypertension: electrocardiogram; urinalysis; blood glucose and hematocrit; serum potassium, creatinine (or the corresponding estimated glomerular filtration rate [GFR]), and calcium; and a lipid profile after 9- to 12-hour fast, which includes high density lipoprotein cholesterol and low-density lipoprotein cholesterol, and triglycerides. Optional tests include measurement of urinary albumin excretion or albumin/creatinine ratio.12
  • Laboratory studies are helpful in establishing the etiology of hypertension, quantitating severity of target organ damage, and monitoring the adverse effects of therapy.
  • Blood urea nitrogen (BUN) and creatinine levels are elevated in patients with renal failure.
  • Hypokalemia is found in patients with primary hyperaldosteronism and in patients with secondary hyperaldosteronism, Cushing disease, and Bartter syndrome. Hypokalemia is most useful in leading to further diagnostic studies if the patient has not received diuretics.
  • Plasma renin activity generally is depressed and serum aldosterone level is elevated in patients with primary hyperaldosteronism.
  • Twenty-four–hour urinary catecholamine and metanephrine levels are elevated in patients with pheochromocytoma.
  • Elevated 24-hour urinary free cortisol and failure to suppress an early morning serum cortisol level after an overnight dexamethasone suppression test are observed in patients with Cushing disease.
  • Thyrotropin levels may be elevated in patients with hypothyroidism and depressed in patients with hyperthyroidism.
  • Other laboratory studies to be ordered depend on clinical judgment regarding the etiology of hypertension.

Imaging Studies

  • Chest radiographs may show the following:
    • Notching of the undersurface of the ribs - Secondary to the development of collateral circulation in coarctation of the aorta
    • Cardiomegaly - Secondary to LV dilatation, in late stages of the disease
    • Cephalization of pulmonary blood flow, Kerley B lines, and alveolar infiltrates - In patients with elevated LV end-diastolic pressure and pulmonary congestion
    • Blunting of costophrenic angle - In patients who develop pleural effusion
  • Computed tomography (CT) scanning, magnetic resonance imaging (MRI), and magnetic resonance angiography of the abdomen and chest show the presence of adrenal masses or evidence of coarctation of aorta.
  • CT scanning and MRI of the heart, although not used routinely, have been shown in experimental studies to quantify LVH.
  • Transthoracic echocardiography (TTE) may be very useful in identifying features of hypertensive heart disease (see Media files 1-4).

    • Two-dimensional echocardiogram of a 70-year-old w...

      Two-dimensional echocardiogram of a 70-year-old woman (parasternal long axis view) showing concentric left ventricular hypertrophy.

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      Two-dimensional echocardiogram of a 70-year-old w...

      Two-dimensional echocardiogram of a 70-year-old woman (parasternal long axis view) showing concentric left ventricular hypertrophy.


    • Two-dimensional echocardiogram of a 70-year-old w...

      Two-dimensional echocardiogram of a 70-year-old woman (parasternal short axis view) showing concentric left ventricular hypertrophy.

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      Two-dimensional echocardiogram of a 70-year-old w...

      Two-dimensional echocardiogram of a 70-year-old woman (parasternal short axis view) showing concentric left ventricular hypertrophy.


    • M-mode echocardiogram of a 70-year-old woman show...

      M-mode echocardiogram of a 70-year-old woman showing concentric left ventricular hypertrophy.

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      M-mode echocardiogram of a 70-year-old woman show...

      M-mode echocardiogram of a 70-year-old woman showing concentric left ventricular hypertrophy.


    • Two-dimensional echocardiogram of a 70-year-old w...

      Two-dimensional echocardiogram of a 70-year-old woman (parasternal short axis view at the aortic valve level) showing mild aortic sclerosis.

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      Two-dimensional echocardiogram of a 70-year-old w...

      Two-dimensional echocardiogram of a 70-year-old woman (parasternal short axis view at the aortic valve level) showing mild aortic sclerosis.

    • Evidence of LVH
      • TTE is more sensitive and specific then ECG for diagnosing the presence of LVH—57% for mild and 98% for severe LVH.
      • LVH is symmetrical, while the hypertrophy of hypertrophic cardiomyopathy is asymmetrical. Definition of the LVH based on echocardiography findings is somewhat controversial in the absence of any criterion standards.
      • On 2-dimensional and M-mode examination, the interventricular septum is thickened, as is the posterior wall (>1.1 cm).
      • LVH is defined quantitatively as an increase in the LV mass or LVMI. Various formulas have been used to calculate LV mass, each with inherent drawbacks.
      • The Troy formula was used in the Framingham Heart study. The ASE-recommended formula for estimation of LV mass from LV linear dimensions (validated with necropsy r 0.90, P.00121) is based on modeling the LV as a prolate ellipse of revolution:
        • LV mass 0.8 X {1.04[(LVIDd+PWTd+SWTd)3-(LVIDd)3]}+ 0.6 g
        • where PWTd and SWTd are posterior wall thickness at end diastole and septal wall thickness at end diastole, respectively. This formula is appropriate for evaluating patients without major distortions of LV geometry (eg, patients with hypertension).
        • In various studies, LVH has been defined either as LV mass greater than 215 g or greater than 225 g. Because LV mass is affected by height, weight, and body surface area, LVMI, defined as LV mass divided by body surface area, more accurately sets the limits for LV mass. Framingham Heart Study data indicate that abnormal LVMI limits are 134 g/m2 for men and 110 g/m2 for women.
    • Evidence of LV diastolic dysfunction as measured by the following:
      • The transmitral flow velocity pattern, characterized by abnormally prolonged isovolumic relaxation time, a reversed "E:A" ratio, and a prolonged deceleration time, is abnormal. The patient may exhibit a pseudonormal pattern during the transition from the impaired relaxation to the restrictive filling phase.
      • The tissue Doppler indices are abnormal. The tissue Doppler profile shows a reversed E:A ratio. This is especially helpful in patients who have a pseudonormal pattern on transmitral flow velocity Doppler studies.
    • Evidence of LV systolic dysfunction
      • The LV is dilated.
      • The LV fractional shortening is low.
      • The LV ejection fraction is low.
      • Systolic dysfunction is present, which is commonly associated with some degree of diastolic dysfunction.
    • Evidence of LA dilatation
    • Evidence of right-sided dilatation: Right-sided chambers may be dilated with some degree of pulmonary hypertension.
    • Evidence of valvular abnormalities, such as aortic sclerosis (on 2-dimensional) and aortic and mitral insufficiency (on color flow and Doppler examination)
  • Nuclear imaging may be useful in screening for the presence of coronary artery disease.

Other Tests

  • Sleep evaluation
  • Additional tests for excluding other secondary causes of hypertension.
  • Twelve-lead ECG may show a variety of abnormalities.
    • Evidence of left atrial enlargement - Broad P waves in limb leads and prominent and wide delayed negative deflection in V1 (see Media files 5-6)

      • ECG of a 47-year-old man with a long-standing his...

        ECG of a 47-year-old man with a long-standing history of uncontrolled hypertension showing left atrial enlargement and left ventricular hypertrophy.

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        ECG of a 47-year-old man with a long-standing his...

        ECG of a 47-year-old man with a long-standing history of uncontrolled hypertension showing left atrial enlargement and left ventricular hypertrophy.


      • ECG of a 46-year-old man with long-standing hyper...

        ECG of a 46-year-old man with long-standing hypertension showing left atrial abnormality and left ventricular hypertrophy with strain.

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        ECG of a 46-year-old man with long-standing hyper...

        ECG of a 46-year-old man with long-standing hypertension showing left atrial abnormality and left ventricular hypertrophy with strain.

    • Conduction abnormalities
      • Of patients with left anterior fascicular block on ECG, 50% had hypertension in one series.
      • As many as 70-80% of patients with LBBB have hypertension.
    • Evidence of LVH on ECG
      • The frequency of LVH on ECG at the time of initial diagnosis varies from 10-100%; in a recent trial, the frequency was 13%.
      • The sensitivity of ECG for diagnosing LVH is limited, 30-57% in patients with severe LVH.
    • Other criteria: Various criteria, differing in sensitivity and specificity, have been used to diagnose LVH, as summarized below. Note that the specificities and sensitivities of all these approaches are far less than those of echocardiography.
      • The Cornell criteria (most sensitive) are (1) RaVL plus an S wave in V3 of greater than 2.8 mV in men and greater than 2 mV in women. The Cornell and Cornell voltage duration (Cornell voltage multiplied by QRS duration) criteria have a sensitivity of as high as 95% and a specificity of as high as 50-60%. A Cornell voltage duration of greater than 2440 mV/ms-1 particularly identified the highest-risk patients.
      • The Sokolow-Lyon criteria are an S wave in V1 plus an R wave in V5 or V6 of greater than 3.5 mV or an R wave in V5 or V6 of greater than 2.6 mV. The sensitivity of these criteria is 25%, with a specificity of close to 95%.
      • The Gubner-Ungerleider criteria are an R wave in I plus an S wave in III of greater than 2.5 mV
Table 1. Romhilt-Estes Criteria (a point score system*)

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Table
Voltage CriteriaPoints
R wave or S wave in any limb lead >0.2 mV or S wave in lead V1 or V2 or R wave in V5 or V6 >0.3 mV3
LV strain (ST and T waves in direction opposite to QRS direction) without digitalis3
LV strain (ST and T waves in direction opposite to QRS direction) with digitalis1
LA enlargement (terminal negativity of P waves in V1 >0.1 mV deep and 0.04 seconds wide)3
Left-axis deviation of greater than -30°2
QRS duration greater than 0.09 seconds1
Intrinsicoid deflection in V5 or V6 >0.05 seconds1
Voltage CriteriaPoints
R wave or S wave in any limb lead >0.2 mV or S wave in lead V1 or V2 or R wave in V5 or V6 >0.3 mV3
LV strain (ST and T waves in direction opposite to QRS direction) without digitalis3
LV strain (ST and T waves in direction opposite to QRS direction) with digitalis1
LA enlargement (terminal negativity of P waves in V1 >0.1 mV deep and 0.04 seconds wide)3
Left-axis deviation of greater than -30°2
QRS duration greater than 0.09 seconds1
Intrinsicoid deflection in V5 or V6 >0.05 seconds1

*Probable LVH is 4 points; definite LVH is 5 points. The sensitivity of these criteria is 50%, with a specificity of close to 95%.

Procedures

Cardiac catheterization is used for diagnosis of coronary artery disease and helps assess the severity of elevated pulmonary artery pressure in patients with heart failure.

Histologic Findings

Gross findings

LVH (concentric) occurs without dilatation of the LV (see Media file 7). The ratio of wall thickness to the radius of the ventricular chamber increases. LV wall thickness may exceed 2 cm, and the heart weight exceeds 500 g. Dilatation of the ventricular chamber, thinning of the walls, and enlargement of the external dimensions of the heart occur with the onset of decompensation.

Gross specimen of the heart with concentric left ...

Gross specimen of the heart with concentric left ventricular hypertrophy.

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Gross specimen of the heart with concentric left ...

Gross specimen of the heart with concentric left ventricular hypertrophy.



Microscopic findings

The earliest changes of hypertensive heart disease include myocyte enlargement, with an increase in their transverse diameters (see Media file 8).

Histologic section of the myocardium showing a cr...

Histologic section of the myocardium showing a cross-section of coronary artery affected by atherosclerosis and myocyte hypertrophy.

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Histologic section of the myocardium showing a cr...

Histologic section of the myocardium showing a cross-section of coronary artery affected by atherosclerosis and myocyte hypertrophy.


At a more advanced stage, cellular and nuclear enlargement (with variation in cell size), loss of myofibrils, and interstitial fibrosis occur (see Media files 9-10).

Histologic section of an autopsy myocardial speci...

Histologic section of an autopsy myocardial specimen from a patient with long-standing hypertension and associated coronary artery disease. The slide shows myocardial hypertrophy, contraction bands (typical of left ventricular hypertrophy), and "car box" nuclei.

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Histologic section of an autopsy myocardial speci...

Histologic section of an autopsy myocardial specimen from a patient with long-standing hypertension and associated coronary artery disease. The slide shows myocardial hypertrophy, contraction bands (typical of left ventricular hypertrophy), and "car box" nuclei.



Histologic section of the heart showing the hyper...

Histologic section of the heart showing the hypertrophied myocytes and fibrosis accompanying left ventricular hypertrophy.

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Histologic section of the heart showing the hyper...

Histologic section of the heart showing the hypertrophied myocytes and fibrosis accompanying left ventricular hypertrophy.

Staging

BP and hypertension itself have been divided into stages.

Table 2. Stages of Elevated BP and Hypertension According to The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

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Table
CategorySystolic BP,
mm Hg		Diastolic BP,
mm Hg
Optimal<120<80
Prehypertension120-13980-89
Stage I140-15990-99
Stage II>160>100
CategorySystolic BP,
mm Hg		Diastolic BP,
mm Hg
Optimal<120<80
Prehypertension120-13980-89
Stage I140-15990-99
Stage II>160>100

When the BP is more than 20/10 mm Hg above the goal, consideration should be given to initiating therapy with 2 drugs, either as separate prescriptions or in fixed-dose combinations.

  • Although hypertensive heart disease typically is not described in various stages, the disease usually progresses in the following sequence: Increased wall stress leads to LVH, which leads to diastolic LV dysfunction, which can be followed by systolic LV dysfunction.
  • The risks of ventricular ectopy, ventricular arrhythmias, sudden cardiac death, and cardiovascular mortality are increased in patients once the LVH develops and in patients with heart failure.

More on Hypertensive Heart Disease

Overview: Hypertensive Heart Disease
Differential Diagnoses & Workup: Hypertensive Heart Disease
Treatment & Medication: Hypertensive Heart Disease
Follow-up: Hypertensive Heart Disease
Multimedia: Hypertensive Heart Disease
References
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Further Reading

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Keywords

left ventricular hypertrophy, congestive heart failure, hypertension, high blood pressure, hyperpiesis, hyperpiesia, angina, myocardial infarction, MI, heart attack, coronary artery disease

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Contributor Information and Disclosures

Author

Kamran Riaz, MD, Clinical Assistant Professor, Department of Internal Medicine, Section of Cardiology, Wright State University School of Medicine
Kamran Riaz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, American Society of Echocardiography, Ohio State Medical Association, and Royal College of Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Aqeel Ahmed, MD, Staff Physician, Department of Pathology, University of Missouri at Kansas City
Aqeel Ahmed, MD is a member of the following medical societies: American Society for Clinical Pathology
Disclosure: Nothing to disclose.

Medical Editor

Hanumant Deshmukh, MD †, Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Yasmine Subhi Ali, MD, MSCI, Assistant Professor of Medicine, Director of Preventive Cardiology, Director of Echocardiography, Meharry Medical College; Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine
Yasmine Subhi Ali, MD, MSCI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Echocardiography, American Society of Nuclear Cardiology, and National Lipid Association
Disclosure: Pfizer I own a small number of shares of Pfizer stock. These were NOT given to me by Pfizer, but rather purchased by myself as a personal investor for my diversified investment portfolio. None

 
 
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