Hypertensive Heart Failure

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5 Hypertensive Heart Failure

Fay Y. Lin, Richard B. Devereux

Left Ventricular Hypertrophy

• Myocardial hypertrophy is a response to increased LV wall stress in accordance with Laplace’s law.

• Laplace’s law describes the relationship of wall tension (T) to the transmural pressure difference (P), the radius (r) and thickness (h) of the LV (Figure 5-1).

• High pressure stimulates compensatory increases in wall thickness. Increased volume dilates the cavity and causes higher wall tension for constant pressure, stimulating compensatory LV hypertrophy (LVH) (Figure 5-2).

• Both volume and pressure load influence LVH in hypertension.

• LVH and left ventricular mass (LVM) are strong, independent predictors of all-cause death, congestive heart failure, sudden cardiac death, and other cardiovascular events.

Figure 5-1 Laplace’s law describes the relationship of wall tension and pressure to ventricular size and thickness.

Figure 5-2 Gross pathology of LVH.

How to Evaluate LV Mass

• LV mass may be evaluated using linear, two-dimensional (2D), or three-dimensional (3D) measurements. LV mass is measured by subtracting LV cavity volume from LV epicardial volume to obtain LV myocardial volume, and multiplication of volume by myocardial density to obtain LV mass.

• LVM quantitation requires adequate endocardial and epicardial definition, and on-axis imaging.

Linear Measurements

Key Points

• Linear measurements of interventricular septal wall thickness (SWT), posterior wall thickness (PWT), and LV diastolic internal dimension (LVIDd) should be made from the parasternal long-axis window in end-diastole (Figure 5-3).

• Measurements should be taken at the level of the LV minor axis, at the papillary muscle level.

• Linear measurements can be made directly from 2D images or using 2D-targeted M-mode echocardiography. M-mode recordings aligned perpendicular to the LV long axis may facilitate exclusion of trabeculae and false tendons from the LV wall.

• Linear measurements should be made from leading edge to leading edge.

• To avoid inclusion of RV and LV trabeculae, measurements should be taken from the most rapidly moving myocardial interface.

• Oblique imaging planes may overestimate cavity size and wall thickness (Figure 5-4).

• LVM may be estimated by the following necropsy-validated formula (Figure 5-5):

Figure 5-3 LV linear measurements. A, The endocardial interface (arrows) should be measured from the most rapidly moving myocardial interface to avoid inclusion of RV and LV trabeculae. B, Measurements should be taken at the level of the LV minor axis. C, 2D-directed M-mode measurements in the same patient using the most rapidly moving myocardial interface.

Figure 5-4 3D echocardiography illustrates potential pitfalls in LV measurement due to off-axis imaging. The green, red, and blue lines represent the four-chamber (A), two-chamber, and short-axis planes, respectively, from the 3D volume (B). A correctly oriented LV minor axis plane (C) results in a short-axis image (D) with smaller diameter and thinner apparent wall thickness than an off-axis plane (E and F), without grossly visible differences in short axis.

Figure 5-5 Echocardiographic LV mass has a high correlation (r ≥ 0.90) versus necropsy in humans and experimental animals.

(Reproduced with permission from Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings. Am J Cardiol. 1986;57:450-458.)

• Relative wall thickness (RWT) may be estimated as:

2D Measurement of LVM

Key Points

• Epicardial and endocardial contours are traced in the 4-chamber and 2-chamber views at end-diastole.

• Traced contours are used to calculate LV volumes by the biplane Simpson method.

• Foreshortening of the LV apex can systematically underestimate LV cavity volumes, with variable impact on LVM measurement.

3D Measurement of LVM

Key Points

• 3D measurement requires high-quality 3D LV volume acquisition with clear endocardial and epicardial interfaces.

• This may be unobtainable with atrial fibrillation or poor acoustic windows.

• Echocardiographic contrast may be useful for poor endocardial definition.

• Select anatomically correct 2- and 4-chamber views with the largest long-axis dimensions (Figure 5-6).

• Epicardial and endocardial contours are traced in the 4-chamber and 2-chamber views at end-diastole. Traced contours are used to calculate LV volumes by use of the biplane Simpson formula similar to 2D measurement of LVM.

• 3D measurement has lower interobserver variability than 2D measurement (Figure 5-7).

Figure 5-6 Reorientation of planes using 3D echocardiography. The four-chamber (A, green), two-chamber (B, red), and short-axis (C, blue) planes are identified by corresponding lines in other projections (D). The short-axis plane is defined by positioning the blue line in both apical views (A and B) at the midpapillary muscle level perpendicular to the long axis of the ventricle. The apical views are iteratively selected by repositioning the red and green lines to pass through the midcavity to the apex, ensuring that the resulting views have the largest long-axis dimension. End-diastolic epicardial and endocardial contours are traced in 4-chamber and 2-chamber views to obtain myocardial volume and mass.

(Reproduced with permission from Mor-Avi V, Sugeng L, Weinert L, et al. Fast measurement of left ventricular mass with real-time three-dimensional echocardiography: Comparison with magnetic resonance imaging. Circulation. 2004;110:1814-1818.)

Figure 5-7 3D measurement of LVM has lower interobserver variability than 2D measurement of LVM. Additionally, 3D measurement of LVM has high agreement with measurement by cardiac magnetic resonance imaging (CMRI).

Definition of LVH and Abnormal LV Geometry

LV Geometry (Figure 5-8)

Figure 5-8 Definition of abnormal LV geometry.

Key Points

• LV geometry is defined by RWT and LV mass (Figure 5-9).

• Normal LVM with normal or increased RWT is classified as normal LV geometry or concentric LV remodeling.

• LVH (increased LV mass) with normal or increased RWT is classified as eccentric or concentric hypertrophy.

• LV geometry has incremental value for prognostication of mortality (Figure 5-10) and to heart failure events, all-cause mortality, and composite cardiac events (Figures 5-11 and 5-12).

Figure 5-9 Hemodynamic and geometric profiles in hypertensive patients with four patterns of LV geometry. Compared with normal geometry, concentric LV remodeling is associated with lower cardiac output, as lower end-diastolic volume limits SV for the same EF. Concentric LVH is associated with higher systolic blood pressure. Eccentric LVH is associated with higher systolic blood pressure and cardiac output, as higher end-diastolic volumes increase SV for the same EF.

(Reproduced with permission from Ganau A, Devereux RB, Roman MJ, et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992;19:1550-1558.)

Figure 5-10 Relationship of LV geometry to mortality in patients with uncomplicated hypertension. Concentric hypertrophy (CH) carries the greatest risk, followed by eccentric hypertrophy (EH) and concentric remodeling (CR). NL, normal.

(Adapted with permission from Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991;114:345-352.)

Figure 5-11 LVM and LVH raise the risk of incident heart failure events in the Multi-Ethnic Study of Atherosclerosis.

(Reprinted with permission from Bluemke DA, Kronmal RA, Lima JA, et al. The relationship of left ventricular mass and geometry to incident cardiovascular events: The MESA (Multi-Ethnic Study of Atherosclerosis) study. J Am Coll Cardiol. 2008;52:2148-2155.)

Figure 5-12 Relationship of LV geometry to all-cause mortality and composite cardiac events (cardiovascular death, recurrent myocardial infarction, heart failure, stroke, and resuscitated sudden death) post myocardial infarction in the VALIANT study. Concentric hypertrophy has the highest risk, followed by eccentric hypertrophy and then concentric remodeling.

(Reproduced with permission from Verma A, Meris A, Skali H, et al. Prognostic implications of left ventricular mass and geometry following myocardial infarction: The VALIANT (VALsartan In Acute myocardial iNfarcTion) Echocardiographic Study. JACC Cardiovasc Imaging. 2008;1:582-591.)

Clinical Vignettes

Case 1

A 48-year-old diabetic, hypertensive man with unlimited exercise tolerance was referred to echocardiography to evaluate atypical chest pain. His blood pressure was 160/100 mm Hg on valsartan and hydrochlorothiazide. He was mildly overweight with a normal exam. The LV ejection fraction (LVEF) was normal with normal valvular function. On echocardiographic exam, LV geometry was normal (Figure 5-13A):

• SWT 1.0 cm, LVIDd 4.6 cm, PWT 1.0 cm

• LVM 136 gm, LVM index (LVMI) 69 gm/m² (normal)

• RWT 0.35% (normal)

• LVEF was normal without wall motion abnormalities. Left atrial (LA) size was normal with a diameter of 4.0 cm.

• Off-axis imaging increased the apparent cavity diameter and wall thickness.

Figure 5-13 Normal LV geometry (A) and normal mitral filling pattern (B) in a diabetic, hypertensive man with atypical chest pain. MV, mitral valve; TDI, tissue Doppler imaging.

The mitral filling pattern was also normal (Figure 5-13B):

• E/A 1.2, deceleration time 178 ms

• Isovolumic relaxation time (IVRT) 77 ms

• Septal E′ 7 cm/s, E/E′ 8

• Lateral E′ 17 cm/s, E/E′ 3

The patient went on to nuclear stress testing demonstrating normal exercise electrocardiogram (ECG) and perfusion imaging, but severe exercise-induced hypertension. Blood pressure medication was increased.

Case 2

A 60-year-old man with hypertension, myelofibrosis, and multiple falls underwent echocardiography during evaluation of presyncope. His blood pressure was 131/77 mm Hg on amlodipine and captopril. He was normal weight with a normal exam. His hemoglobin was 8.0 gm/dL. The LVEF was normal with normal valvular function (Figure 5-14A). On echocardiographic exam:

• SWT 0.8 cm, LVIDd 4.2 cm, PWT 0.8 cm

• LVM 136 gm, LVMI 69 gm/m² (normal)

• RWT 0.38% (normal)

• LA diameter 4.0 cm (normal)

Figure 5-14 Normal LV geometry (A) and normal mitral filling pattern for age (B) in a 60-year-old hypertensive man with presyncope.

The mitral filling pattern was normal for age (Figure 5-14B):

• E/A 0.9, deceleration time 292 ms

• IVRT 103 ms

• Septal E′ 8 cm/s, E/E′ 8

• Lateral E′ 9 cm/s, E/E′ 7

Despite the E/A reversal and prolonged deceleration time and IVRT, tissue Doppler velocities were normal for age and there was no evidence of elevated LV filling pressures. The inferior vena cava (IVC) had normal respiratory variation, consistent with right atrial (RA) pressures between 5 and 10 mm Hg. An E/E′ ratio ≤ 8 was consistent with normal LV filling pressures. The patient was diagnosed with seizure by electroencephalography.

Case 3

A 75-year-old woman with hypertension underwent echocardiography during evaluation of palpitations. She had unlimited exercise tolerance with no other symptoms. Her blood pressure was 135/70 mm Hg on atenolol. She was normal weight with a I/VI systolic murmur at the left upper sternal border and trace lower extremity edema. The LVEF was normal with normal valvular function. There was mild mitral and aortic annular calcification. Estimated glomerular filtration rate (GFR) by MDRD was 57 mL/min (Figure 5-15A). On echocardiographic exam, LV geometry was consistent with borderline eccentric hypertrophy:

• SWT 1.0 cm, LVIDd 4.9 cm, PWT 0.9 cm

• LVM 164 gm, LVMI 98 gm/m² (LVM/h^2.7 of 46.2 gm/m² is borderline LVH)

• RWT 0.37% (normal)

• LA size was normal.

Figure 5-15 Borderline eccentric LVH (A) and normal mitral filling pattern for age (B) in an elderly, hypertensive woman with palpitations. PV, pulmonary valve.

The filling pattern was normal for age (Figure 5-15B):

• E/A 0.9, deceleration time 243 ms

• IVRT 116 ms

• S-dominant pulmonary venous inflow, consistent with decreased ventricular compliance

• Septal E′ 6 cm/s (normal for age); E/E′ 13

• Lateral E′ 7 cm/s (normal for age); E/E′ 11 ⁶

The IVC was normal in size with normal respiratory collapse. She had an abnormal relaxation pattern with E/A reversal and prolonged deceleration time and IVRT, and S-dominant pulmonary venous flow, which may be consistent with normal aging (Figure 5-16).

Figure 5-16 Echocardiographic LVH increases the risk of atrial fibrillation.

(Reprinted with permission from Verdecchia P, Reboldi G, Gattobigio R, et al. Atrial fibrillation in hypertension: Predictors and outcome. Hypertension. 2003;41:218-223.)

Case 4

A 94-year-old woman with diabetes was referred to evaluate dyspnea on exertion. She had a block exercise tolerance without other signs or symptoms of heart failure. Her blood pressure was 112/76 mm Hg on no antihypertensives. Her brain natriuretic peptide (BNP) was 23. An ECG demonstrated sinus tachycardia. The LVEF was normal with mild aortic stenosis. LA size was normal for age and body size (Figure 5-17A). On echocardiographic exam, the LV geometry was consistent with concentric remodeling:

• SWT 1.1 cm, LVIDd 4.0 cm, PWT 1.0 cm

• LVM 135 gm, LVMI 83 gm/m² (normal)

• RWT 0.50% (concentric)

Figure 5-17 Concentric remodeling (A) and evidence of elevated LV filling pressures (B) in a woman of advanced age with dyspnea on exertion.

The stroke volume (SV) was relatively low at 55 mL, with maintenance of a normal cardiac index of 3.4 L/min/m² with tachycardia.

There was evidence of elevated LV filling pressures (Figure 5-17B):

• E/A 0.7, deceleration time 242 ms, IVRT 129 ms

• S-dominant pulmonary vein flow

• Septal E′ 5 cm/s, E/E′ 20; lateral E′ 3 cm/s, E/E′ 33

LV filling parameters were suggestive of heart failure with a normal EF ⁷ (Figure 5-18).

Figure 5-18 LV morphology of heart failure with normal ejection fraction (HFNEF). Relative wall thickness (RWT, red line) is significantly higher with HFNEF than in asymptomatic hypertensive or normal patients in the community.

(Adapted with permission from Borlaug BA, Melenovsky V, Redfield MM, et al. Impact of arterial load and loading sequence on left ventricular tissue velocities in humans. J Am Coll Cardiol. 2007;50:1570-1577.)

Case 5

A 93-year-old woman with hypertension and a history of non-sustained ventricular tachycardia was referred to echocardiography for syncope. Her blood pressure was 94/56 mm Hg before and 115/70 mm Hg after hydration. The LVEF was hyperdynamic with moderate mitral and tricuspid regurgitation (Figure 5-19A). On echocardiographic exam, LV geometry was consistent with concentric remodeling:

• SWT 1.2 cm, LVIDd 4.0 cm, PWT 1.0 cm

• LVM 146 gm, LVMI 92 gm/m², RWT 0.5%

Figure 5-19 Concentric remodeling (A) evidence of elevated filling pressures (B) in a woman of advanced age with syncope.

Filling parameters were consistent with abnormal relaxation and elevated LV filling pressures (Figure 5-19B):

• E/A 0.7, deceleration time 261 ms

• Septal E′ 3 cm/s, E/E′ 33; lateral E′ 3 cm/s, E/E′ 33

• Tricuspid regurgitation (TR) velocity 2.8 m/s, consistent with pulmonary artery (PA) systolic pressure of 37 to 41 mm Hg.

The IVC was normal in size with normal respiratory variation, consistent with RA filling pressures of 5 to 10 mm Hg.

Case 6

A 41-year-old man with stage V chronic kidney disease secondary to hypertension was referred to echocardiography for an abnormal ECG. He had an unlimited exercise tolerance with no symptoms of heart failure. His blood pressure was 140/93 mm Hg on amlodipine, labetalol, furosemide, hydralazine, and isosorbide dinitrate. On exam, he had trace lower extremity edema without jugular venous distention or crackles. The LVEF was normal with normal valvular function. The LA was severely dilated by volume measurement (Figure 5-20A). On echocardiographic exam, LV geometry was consistent with concentric hypertrophy:

• SWT 1.3 cm, LVIDd 4.8 cm, PWT 1.3 cm

• LVM 245 gm, LVMI 142 gm/m², RWT 0.54%

Figure 5-20 Concentric hypertrophy (A) and evidence of elevated filling pressures (B) in an asymptomatic hypertensive man with stage V chronic kidney disease.

LV filling parameters were consistent with pseudonormalization and mildly elevated LV filling pressures (Figure 5-20B):

• E/A 1.3, deceleration time 221 ms

• Septal E′ 4 cm/s, E/E′ 21; lateral E′ 6 cm/s, E/E′ 12

• Pulmonary venous inflow with mild systolic blunting, increased A reversal

• Peak pulmonic regurgitation (PR) velocity 1.0 m/s, consistent with PA diastolic pressure of 19 to 24

• LV outflow tract (LVOT) velocity-time integral (VTI) 26 cm and SV 106 mL, consistent with volume overload

The IVC was dilated without respiratory variation, consistent with elevated RA filling pressures of 15 to 20 mm Hg.

Case 7

A 64-year-old man was referred for echocardiography to evaluate LV function after discharge from hospitalization for a hypertensive emergency. He had an unlimited exercise tolerance and no symptoms. His blood pressure was 144/66 mm Hg on carvedilol, losartan, amlodipine, and furosemide. His estimated GFR was 73 mL/min. LV function was normal with normal valvular function. The LA was dilated, with an LA volume index of 47 mL/m². Two years later, he had progression of renal insufficiency and was referred to echocardiography for lower extremity edema. Exercise tolerance was unlimited. The blood pressure was 160/88 mm Hg on carvedilol, amlodipine, furosemide, isosorbide dinitrate and hydralazine in lieu of losartan due to hyperkalemia (Figure 5-21A).

Figure 5-21 Concentric hypertrophy in a hypertensive emergency (A) and improved left ventricular filling pressure with medical therapy and LVH regression (B) in a hypertensive man.

LV geometry in 2008 was consistent with concentric LVH:

• 2008 SWT 1.6 cm, LVIDd 5.8 cm, PWT 1.5 cm

• 2008 LVM 425 gm, LVMI 195 gm/m², RWT 0.52%

LV geometry in 2010 was consistent with less severe concentric LVH:

• 2010 SWT 1.6 cm, LVIDd 5.1 cm, PWT 1.5 cm

• 2010 LVM 349 gm, LVMI 156 gm/m², RWT 0.59%

LV filling in 2008 was consistent with pseudonormalization and possibly elevated LV filling pressures (Figure 5-21B):

• 2008 E/A 1.2, deceleration time 215 ms, IVRT 85 ms

• 2008 Septal E′ 3 cm/s, E/E′ 23; lateral E′ 5 cm/s, lateral E/E′ 14

• 2008 Pulmonary veins demonstrated very mild systolic blunting.

LV filling in 2010 was consistent with abnormal relaxation and normal LV filling pressures:

• 2010 E/A 0.8, deceleration time 341 ms, IVRT 95 ms

• 2010 Septal E′ 3 cm/s, E/E′ 17; lateral E′ 8 cm/s, lateral E/E′ 9

• 2010 Pulmonary veins were S dominant.

Figure 5-22 shows the association of in-treatment LV mass with risk of cardiovascular events.

Figure 5-22 Association of in-treatment LV mass with risk of cardiovascular (CV) events in the LIFE trial: results of Cox multivariable proportional hazards analysis. Hazards are adjusted for baseline LVMI, treatment with atenolol or losartan, and blood pressure lowering.

(Adapted with permission from Devereux RB, Wachtell K, Gerdts E, et al. Prognostic significance of left ventricular mass change during treatment of hypertension. JAMA. 2004;292:2350-2356.)