Systemic Hypertension

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Definition

Hypertensive heart disease is characterized by cardiac hypertrophy in response to increased cardiac afterload. This results in systolic and diastolic dysfunction as well as other structural abnormalities. These in turn manifests clinically as arrhythmias and symptomatic heart failure.[1] Echocardiography can demonstrate many of the effects of hypertension on cardiac function and structure.

Left Ventricular Hypertrophy

Left ventricular hypertrophy (LVH) is recognised as an independent predictor of morbidity and mortality. [2] [3] [4] The prevalence in hypertensive patients ranges from 36% to 41%.[5] LVH is essentially an increase in left ventricular (LV) mass. Methods to measure LV mass include Devereux’s Formula[6] and the Area Length Method.[7]


Inter-ventricular septal thickness and posterior wall thickness as well as the end-diastolic diameter can be measured using m-mode or 2D echocardiography. Devereux’s formula can then be used to estimate left ventricular mass:


LV mass(g) = 0.80 [1.04 {(PWT+LVID+SWT)3 - LVID3}] + 0.6


The Area Length Method can be used for both 2D and 3D echocardiography to estimate left ventricular mass:


LV mass(g) =1.05 X {5/6 (AEpi X LEpi) - (AEndo X LEndo)}


Indexing for body size by dividing LV mass by body surface area should be carried out for both methods.


Relative wall thickness (RWT) allows further classification of LV mass[8] [9]increase as either concentric hypertrophy (RWT >0.42) or eccentric hypertrophy (RWT ≤0.42):


RWT = 2×PWT/LVID


Mmode.jpeg
Estimation of left ventricular mass by m-mode echocardiography Parasternal long and short axis views demonstrating severe left ventricular hypertrophy in a young man presenting with secondary hypertension

Diastolic Dysfunction

Hypertension can lead to diastolic dysfunction which can occur in the presence or absence of LVH. Diastolic dysfunction leads to elevated filling pressures.[10] There is no single measure of diastolic dysfunction. The different techniques need to be considered together to make an overall integrated assessment.



Pulsed-wave doppler assessment of transmitral flow should form the basis of assessment. From this peak early diastolic filling velocity (E) and peak late diastolic filling velocity (A), can be obtained as well as E:A ratio. Other important information available from this technique is the E wave deceleration time and the isovolumetric relaxation time.[11]


E wave deceleration time reflects LV compliance. In early diastolic dysfunction it increases. However, as progression of diastolic dysfunction occurs and filling pressures rise there is a decrease in the deceleration time. Isovolumetric relaxation time (IVRT) is the time from closure of the aortic valve to opening of the mitral valve. It is measured from a modified apical 4 chamber view which includes the outflow tract and aortic valve. A pulsed- wave doppler signal that simultaneously demonstrates aortic outflow and mitral inflow should be obtained. IVRT is the time interval between the two signals. It is prolonged in early diastolic dysfunction but like the E wave deceleration time becomes shorter as disease progresses.


Tissue Doppler myocardial imaging is the next step and is carried out at the ventricular basal wall at or within 1 cm of the mitral valve leaflet insertion point. Signals should be recorded from lateral and septal walls. This allows assessment of peak early diastolic myocardial velocity (e’) and peak late diastolic myocardial velocity (a’). The E/e’ ratio can then also be calculated from which an estimation of filling pressure can be made.[12]


Left atrial (LA) filling can also be assessed using pulsed-wave doppler interrogation of pulmonary venous flow. This should be looked at in conjunction with the other parameters of diastolic function. Peak systolic pulmonary vein flow velocity (S), peak diastolic pulmonary vein flow velocity (D), peak pulmonary vein atrial reversal velocity (AR) and AR duration (ARdur) can be obtained.


Diastolic dysfunction is classified into stages using the various echocardiographic parameters.

  1. Stage I - Impaired relaxation
  2. Stage II - Pseudo-normalisation
  3. Stage III - Restrictive which can be reversible or fixed


In any assessment of diastolic function the volume status of the patient must be taken into consideration as it influences the findings. Heart rate and rhythm also have an impact. Age is important - it is normal to see some degree of diastolic dysfunction in older patients. A valsalva manoeuvre should be used in order to distinguish the different stages.

Mitral inflow demonstrating E:A ratio of 0.8 with prolonged E wave deceleration of 257 msec in keeping with stage I diastolic dysfunction
Mitral inflow demonstrating E:A ratio of 1.3 and prolonged E wave deceleration time of 218 msec. For tissure doppler see next image.
Tissue doppler related to previous image demonstrating reduced e' to a' ratio in keeping with stage II diastolic dysfunction
Mitral inflow demonstrating E:A ratio of 1.8 and E wave deceleration time of 92 msec in keeping with stage III diastolic dysfunction

Left Atrial Size

As LV pressure rises so too will LA pressure to maintain diastolic filling of the LV. This increases wall tension and leads to chamber dilatation. LA size can therefore be considered a chronic reflection of filling pressures. LA size can be measured by diameter from the parasternal long axis view or alternatively by area or volume from apical views. However, indexed LA volume has been demonstrated to be a more sensitive marker of future cardiovascular events than LA diameter or area.[13] Left atrial volume has also been shown to be a marker for diastolic dysfunction severity.[14] Left atrial enlargement was correlated to blood pressure in the Framingham Heart study.[15] Left atrial volume has been shown to be increased even in those with mild hypertension.[16] Of course the size of the left atrium is of particular clinical relevance with respect to atrial fibrillation and stroke.

Enlarged left atrium by diameter measured from parasternal long axis view
Enlarged left atrium measured by area and volume measured from apical view

Speckle Tracking Echocardiography

Speckle tracking echocardiography (STE) is a means of assessing myocardial function which is largely angle independent and can be done offline after image acquisition. The myocardium scatters the sound waves which generate speckles specific for an area of myocardium. These speckles can be tracked from frame to frame and provide displacement information. Parameters of myocardial function such as velocity, strain and strain rate can then be derived.[17] STE allows the detection of subtle myocardial dysfunction and may be an appropriate tool to assess hypertensive patients who have subclinical disease but are at risk of progression to overt heart failure or even coronary artery disease.


Aortic Disease

Aortic dilatation is frequently seen in hypertensive patients. Studies have demonstrated prevalence rates above 10%.[18] [19] Hypertension is an important risk factor for aortic dissection.[20]

Dilated ascending aorta in an elderly lady with longstanding hypertension

Related Disorders

Finally to mention manifestations of disorders related to hypertension. Echocardiography may detect regional wall motion abnormalities in keeping with coronary artery disease. Systolic function may be depressed as a result. Atrial fibrillation may cause further dilatation of the left atrium. Slow flow may result in increased echogenicity or ‘smoke’, or even a left atrial thrombus particularly in the left atrial appendage.


References

  1. Drazner MH. The Progression of Hypertensive Heart Disease. Circulation. 2011;123:327-334
  2. Casale PN, Devereux RB, Milner M, Zullo G, Harshfield GA, Pickering TG, et al. Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. Annals of internal medicine. 1986 08/;105(2):173-8.
  3. 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. Annals of internal medicine. 1991 03/;114(5):345-52.
  4. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic Implications of Echocardiographically Determined Left Ventricular Mass in the Framingham Heart Study. New England Journal of Medicine. 1990;322(22):1561-6.
  5. Cuspidi C, Sala C, Negri F, Mancia G, Morganti A. Prevalence of left-ventricular hypertrophy in hypertension: an updated review of echocardiographic studies. Journal of human hypertension. 2012 Jun;26(6):343-9.
  6. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation. 1977 April 1, 1977;55(4):613-8.
  7. Reichek N, Helak J, Plappert T, Sutton MS, Weber KT. Anatomic validation of left ventricular mass estimates from clinical two-dimensional echocardiography: initial results. Circulation. 1983 February 1, 1983;67(2):348-52.
  8. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise J, Solomon S, Spencer KT, St John Sutton M, Stewart W; American Society of Echocardiography's Nomenclature and Standards Committee; Task Force on Chamber Quantification; American College of Cardiology Echocardiography Committee; American Heart Association; European Association of Echocardiography, European Society of Cardiology. Recommendations for chamber quantification.Eur J Echocardiogr. 2006 Mar;7(2):79-108.
  9. Ganau A, Devereux RB, Roman MJ, de Simone G, Pickering TG, Saba PS, Vargiu P, Simongini I, Laragh JH. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992 Jun;19(7):1550-8
  10. Brutsaert DL, Sys SU, Gillebert TC. Diastolic failure: pathophysiology and therapeutic implications. Journal of the American College of Cardiology. 1993 Jul;22(1):318-25.
  11. Cohen GI, Pietrolungo JF, Thomas JD, Klein AL. A practical guide to assessment of ventricular diastolic function using Doppler echocardiography. J Am Coll Cardiol. 1996 Jun;27(7):1753-60.
  12. Nagueh MDSF, Middleton KJ, Kopelen HA, Zoghbi WA, Quiñones MA. Doppler Tissue Imaging: A Noninvasive Technique for Evaluation of Left Ventricular Relaxation and Estimation of Filling Pressures. Journal of the American College of Cardiology. 1997;30(6):1527-33.
  13. Tsang TS, Abhayaratna WP, Barnes ME, Miyasaka Y, Gersh BJ, Bailey KR, Cha SS, Seward JB. Prediction of Cardiovascular Outcomes With Left Atrial SizeIs Volume Superior to Area or Diameter? J Am Coll Cardiol. 2006;47(5):1018-1023
  14. Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward JB. Left atrial volume as a morphophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden. Am J Cardiol. 2002 Dec 15;90(12):1284-9.
  15. Vaziri SM, Larson MG, Lauer MS, Benjamin EJ, Levy D. Influence of Blood Pressure on Left Atrial Size: The Framingham Heart Study. Hypertension. 1995 June 1, 1995;25(6):1155-60.
  16. Eshoo S, Ross DL, Thomas L. Impact of Mild Hypertension on Left Atrial Size and Function. Circ Cardiovasc Imaging 2009;2;93-99
  17. Mor-Avi V, Lang RM, Badano LP, Belohlavek M, Cardim NM, Derumeaux G, Galderisi M, Marwick T, Nagueh SF, Sengupta PP, Sicari R, Smiseth OA, Smulevitz B, Takeuchi M, Thomas JD, Vannan M, Voigt JU, Zamorano JL.Current and Evolving Echocardiographic Techniques for the Quantitative Evaluation of Cardiac Mechanics: ASE/EAE Consensus Statement on Methodology and Indications Endorsed by the Japanese Society of Echocardiography. Eur J Echocardiogr (2011) 12 (3): 167-205
  18. Cuspidi C, Negri F, Salvetti M, Lonati L, Sala C, Capra A, Milan A, Danzi GB, Morganti A; Working Group on Heart and Hypertension of the Italian Society of Hypertension. Aortic root dilatation in hypertensive patients: a multicenter survey in echocardiographic practice. Blood Press. 2011 Oct;20(5):267-73
  19. Milan A, Avenatti E, Tosello F, Iannaccone A, Leone D, Magnino C, Veglio F. Aortic root dilatation in essential hypertension: prevalence according to new reference values. J Hypertens. 2013 Jun;31(6):1189-95.
  20. Howard DP, Banerjee A, Fairhead JF, Perkins J, Silver LE, Rothwell PM; on behalf of the Oxford Vascular Study. Population-Based Study of Incidence and Outcome of Acute Aortic Dissection and Premorbid Risk Factor Control 10-Year Results From the Oxford Vascular Study.Circulation. 2013;127:2031-2037.
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