Systemic Hypertension
Systemic hypertension in animals is typically secondary to other diseases with renal failure, diabetes, and hyperthyroidism being the most common (57,58). The definition of what constitutes systemic hypertension is variable. Pressures ranging from 150/90 to 180/100 and up are all defined as hypertensive in various canine studies (59–61). Hypertension is usually defined as systolic blood pressure above 160 or 180 mm Hg in the cat (57,62–67).
Two-Dimensional and M-mode Features
Chronic increases in afterload caused by systemic hypertension leads to compensatory myocardial hypertrophy in order to normalize wall stress (Figures 6.23, 6.24) (61,68–70). Although logic would suggest that the degree of left ventricular hypertrophy would be directly related to the degree of hypertension, studies have shown that the development of hypertrophy does not correlate linearly to the development of pressure (71,72). Other factors including neural and humoral influences play a role in the development of wall thickness to compensate for the elevation in pressure (70,73). Studies have also shown that the elevation in pressure during daily normal activities in patients with eccentric hypertrophy is less than the pressure elevation in patients with concentric hypertrophy (74).
Concentric or eccentric hypertrophy may be seen with systemic hypertension.
Figure 6.23 Chronic systemic hypertension leads to compensatory left ventricular hypertrophy. This dog with mitral regurgitation has excessive hypertrophy (increased VSd/LVd) for the degree of dilation and was found to be hypertensive. VSd = ventricular septal thickness in diastole, LVd = left ventricular chamber size in diastole.
Figure 6.24 Concentric left ventricular hypertrophy without dilation is seen in this dog with systemic hypertension secondary to a pheochromocytoma. RV = right ventricle, VS = ventricular septum, LV = left ventricle, AO = aorta, LA = left atrium, LVW = left ventricular wall.
Systemic hypertension in cats causes overall alterations in left ventricular shape, concentric left ventricular hypertrophy involving the septum and the free wall, and a small left ventricular chamber size. The type of hypertrophic pattern varies in hypertensive cats, from asymmetric and symmetric hypertrophy involving the septum or free wall, eccentric hypertrophy, and hypertrophy that involves only the base of the interventricular septum. This hypertrophy cannot be differentiated from that seen in hypertrophic cardiomyopathy. Several echocardiographic studies in cats with systemic hypertension showed the following forms of left ventricular hypertrophy (57,75,76). Some cats showed no ventricular changes from normal (15–52%), other cats showed concentric hypertrophy that was symmetric (15.8–32%) or asymmetric (33–48%). Of the asymmetric patterns of hypertrophy, more displayed hypertrophy of the free wall (10–41%) than hypertrophy of the septum (5.3–39%). Eccentric
hypertrophy, which means a dilated left ventricular chamber with or without hypertrophic changes of the septum or wall, was seen in 13% of cats with systemic hypertension (57). Localized septal hypertrophy at the base of the interventricular septum was the only hypertrophic change seen in a number of cats although this change may be seen in normal older cats (Figure 6.25) (57,64). Although the highest blood pressure was seen in cats with eccentric hypertrophy in one study, there is no statistical difference between the types of hypertrophy and the degree or type of hypertrophy and level of blood pressure elevation in any study in the cat (57,64,75,76). It did appear that cats with eccentric enlargement were younger than the rest of the hypertensive cats (57).
Figure 6.25 Localized septal hypertrophy at the base of the interventricular septum was the only hypertrophic change seen in a number of cats with systemic hypertension. This change may be seen in normal older cats. RV = right ventricle, VS = ventricular septum, AO = aorta, LV = left ventricle LVW = left ventricular wall, LA = left atrium.
Although not studied in cats, there is a greater risk of cardiovascular-related death in human patients with hypertrophy, and the degree of septal thickness is considered to be is one of the most important two-dimensional and M-mode predictors of cardiac death secondary to systemic hypertension (77). The degree of hypertrophy and its variable appearance seen in cats with hypertension may be affected by the chronicity. Studies in dogs have shown that hypertrophy develops over the course of about 6 weeks in response to the hypertension (71). The degree of variability in hypertrophic patterns or the lack there of in cats with hypertension make echocardiography an unlikely screening method. Having said this however, it is probably wise to check blood pressure in an animal that shows unexplained hypertrophy on an echocardiographic study.
Systolic dysfunction is also present in hypertensive human patients. Studies in dogs show that systolic function is preserved, although chronicity was not looked at (71,78,79). Eventual myocardial failure may be anticipated as wall stress becomes elevated (80). Systolic dysfunction occurs after the onset of diastolic impairment (68). Fractional shortening cannot be used as an indicator of systolic dysfunction in hypertensive hearts. Increases in systolic and eventually diastolic chamber sizes as well as decreased systolic thickening of the wall and septum indicate that systolic dysfunction is present despite normal fractional shortenings. Congestive heart failure is the result (61,68,69,73,81,82). This systolic impairment may be secondary to impaired myocardial perfusion, the result of changes in the
small coronary vessels or increased afterload and wall stress in patients without adequate compensatory hypertrophy (69,73). When hypertension is treated appropriately, hypertrophy will regress and diastolic function will improve. Improvement of diastolic function as hypertrophy regresses is secondary to the reduced afterload and better rate of myocardial relaxation (68). Systolic function determined with M-mode echocardiography is variable in cats, and although most have normal function, fractional shortening ranges from low to normal and high (57,75).
Left atrial size in cats with hypertension is usually normal but may be large in some. This may be secondary to ventricular remodeling, diastolic failure, or mitral regurgitation (75,76). Although the degree of left ventricular hypertrophy does not correlate with the degree of hypertension, ascending aortic size in cats does. An M-mode measurement at the level of the aortic valve may not reflect this change (64). Two-dimensional assessment of the long-axis left ventricular outflow view is necessary to document this dilation, and comparison of the ascending aorta to the aorta at the level of the annulus is necessary (Figure 6.26). It can be used to differentiate cats with systemic hypertension from those without (64). The aorta is measured at the annulus and the sinus of Valsalva, as well as at the sinotubular junction and the ascending aorta just beyond the sinotubular junction. Measurements at the sinotubular junction and the ascending aorta were larger in all cats with systemic hypertension, while measurements taken at the valve annulus and the sinus were no different in hypertensive cats than normal cats. Normal cats have two-dimensional measurements of 7.6 ± 0.6 mm at the sinotubular junction and the ascending aorta while cats with systemic hypertension had measurements of 9.2 ± 1.1 mm and 9.7 ± 1.2 mm, respectively. Ratios of the sinotubular dimension to the aortic annulus and the ascending aorta to annulus were 1.06 ± 0.1 and 1.05 ± 0.1, respectively, in normal cats while hypertensive cats had ratios of 1.26 ± 0.1 and 1.34 ± 0.1, respectively (64). No healthy cat of any age had a sinotubular to aortic annulus ratio of greater than 1.25. In man studies have shown that aortic root dilation in association with increased left ventricular mass is associated with systolic dysfunction and potentially a poorer prognosis than patients without aortic root dilation and increased mass (83).
Feline
Systemic hypertension
Sinotubular dimension : aortic annulus
1.26 ± 0.1
Ascending aorta : aortic annulus
1.34 ± 0.1
Normal blood pressure
Sinotubular junction : aortic annulus
Always <1.25
Figure 6.26 The ascending aorta is measured at the annulus (1), the sinus of Valsalva (2), the sinotubular junction (3), and the ascending aorta just beyond the sinotubular junction (4). Measurements at the sinotubular junction and the ascending aorta are larger in all cats with systemic hypertension. No healthy cat of any age has a sinotubular to aortic annulus ratio of greater than 1.25. In this cat the ratio of sinotubular junction (7.05 mm) to aortic annulus (6.92 mm) is 1.02. LV = left ventricle, AO = aorta.
Spectral Doppler
Diastolic dysfunction in the setting of systemic hypertension has not been evaluated in animals but has been documented as an early change in man with systemic hypertension before any hypertrophic changes or systolic failure have occurred (84). One study showed that transmitral E:A ratio decreased, pulmonary venous S:D ratio increased, pulmonary venous A reversal flow increased in duration, and isovolumic relaxation time increased in patients that developed mild hypertension over the course of a few years (85).
Human patients often present in left-sided congestive heart failure secondary to systemic hypertension. Previously this was thought to be the consequence of impaired systolic function or exacerbated mitral regurgitation. This was found not to be the case in many patients however, and diastolic failure has been documented as a cause of left heart failure secondary to the presence of systemic hypertension (86). The transmitral filling pattern in these patients reflects impaired relaxation but returns to a pseudonormal or restrictive pattern after treatment for heart failure (85).
Both a restrictive filling pattern and a pseudonormal filling pattern are associated with poor prognosis in human patients with systemic hypertension. This elevation in left ventricular filling pressure is thought to be secondary to hypertrophy, fibrosis, scaring, and increased wall stress. These transmitral flow patterns have the highest predictive value for cardiac-related mortality, over any other echocardiographic parameter, including tissue Doppler. This parameter has not been studied in animals with systemic hypertension (77).
Increased isovolumic relaxation time (IVRT) is a common finding in humans with systemic hypertension. This parameter correlates highly with the degree of left ventricular mass but not necessarily with the degree of wall thickness, and helped define diastolic dysfunction in the pseudonormal group of transmitral valve flow (87). The increase in IVRT is not found in athletes with left ventricular hypertrophy (69,73,81).
Continuous-wave Doppler of mitral regurgitant flow can be used to indirectly determine left ventricular and systemic systolic pressure (Figure 6.27) (88). Alignment of the Doppler beam parallel with the regurgitant jet is imperative, otherwise systemic blood pressure will be underestimated. Adding an estimated left atrial pressure to the calculated pressure gradient will yield the approximate systemic systolic pressure. If left atrial size is increased, this method is less accurate and these animals can not have any outflow obstruction. It can be used to help in situations where peripheral
blood pressure measurements are low and a regurgitant jet pressure gradient can be used to confirm pressure that is more normal. In the presence of mild to moderate mitral regurgitation where proximal flow acceleration is negligible, Doppler-derived systolic pressure can help confirm the diagnosis of systemic hypertension when a peripheral blood pressure cannot be obtained or is thought to be inaccurate (88).
Figure 6.27 Spectral Doppler evaluation of a mitral regurgitant jet can provide information about systemic pressures. The pressure gradient reflects left ventricular driving pressures and systolic systemic pressures when there is no obstruction to outflow. Here the gradient suggests that left ventricular pressure is at least 193 mm Hg, and in the absence of left ventricular outflow obstruction (normal aortic flow velocity), systemic pressures are at least 193 mm Hg.
Tissue Doppler Imaging
Diastolic dysfunction has been documented in systemically hypertensive human patients. Tissue Doppler diastolic annular velocity has been shown to be predictive of cardiovascular mortality in these patients (77). Significantly lower S′ and E′ myocardial annular velocities, especially E′, at both the lateral wall and the septum on four-chamber apical views are associated with poor prognosis in man (77).
Tissue Doppler has been reported in one case of systemic hypertension in a dog. Longitudinal systolic myocardial motion (S′) was depressed in this dog while radial systolic myocardial motion was normal (89). This dog had eccentric left ventricular enlargement and normal fractional shortening, and tissue Doppler imaging was the only indicator of possible systolic dysfunction involving the longitudinal fibers. Longitudinal fibers are thought to be more susceptible to ischemia and fibrosis as compared to radial fibers (90). This evidence of systolic dysfunction using TDI has been documented in man without a decrease in fractional shortening or radial fiber dysfunction as well (90). The dog in this study did have an increased left ventricular systolic dimension, which is usually considered to be an indicator of systolic myocardial dysfunction.
References
1.Bach JF, Rozanski EA, MacGregor J, et al. Retrospective evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs. J Vet Int Med 2006;20: 1132–1135.
2.Johnson L, Boon J, Orton E. Clinical characteristics of 53 dogs with Doppler-derived evidence of pulmonary hypertension: 1992–1996. J Vet Intern Med 1999;13: 440–447.
3.MacDonald KA, Johnson LR. Pulmonary hypertension and pulmonary thromboembolism. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 6 ed. St. Louis: Elsevier Saunders, 2005;1284–1288.
4.Rich S. Pulmonary hypertension. In: Braunwald E, ed. A Textbook of Cardiovascular Medicine. 5 ed. Philadelphia: W. B. Saunders, 1997;780–806.
5.Chiavegato D, Borgarelli M, D’Agnolo G, et al. Pulmonary hypertension in dogs with mitral regurgitation attributable to myxomatous valve disease. Vet Rad and Ultrasound 2009;50:253–258.
6.Kim NHS. Diagnosis and evaluation of the patient with pulmonary hypertension. Cardiol Clin 2004;22:367–373.
7.Kittleson M, Kienle R. Pulmonary arterial and systemic arterial hypertension. In: Kittleson M, Kienle R, eds. Small Animal Cardiovascular Medicine. Saint Louis: Mosby, 1998;433–449.
8.Serres FJ, Chetboul V, Tissier R, et al. Doppler echocardiography-derived evidence of pulmonary arterial hypertension in dogs with degenerative mitral valve disease: 86 cases (2001–2005). Journal of the American Veterinary Medical Association 2006;229:1772–1778.
9.Schober KE, Baade H. Doppler echocardiographic prediction of pulmonary hypertension in west highland white terriers with chronic pulmonary disease. Journal of Veterinary Internal Medicine 2006;20:912–920.
10.Glaus TM, Tomsa K, Hassig M, et al. Echocardiographic changes induced by moderate to marked hypobaric hypoxia in dogs. Vet Rad and Ultrasound 2004;45:233–237.
11.Johnson L. Diagnosis of pulmonary hypertension. Clin Tech Sm Anim Prac 1999;14:231–236.
12.Sherman S. Cor pulmonale. Postgrad Med 1992;91:227–236.
13.Serres F, Chetboul V, Gouni V, et al. Diagnostic value of echo-Doppler and tissue Doppler imaging in dogs with pulmonary arterial hypertension. J Vet Intern Med 2007;21:1280–1289.
14.Lombard C, Buergelt C. Echocardiographic and clinical findings in dogs with heartworm-induced cor pulmonale. Comp Cont Ed 1983;5:971–980.
15.Atkins C, Keene B, McGuirk S. Pathophysiologic mechanism of cardiac dysfunction in experimentally induced heartworm caval syndrome in dogs: an echocardiographic study. Am J Vet Res 1988;49:403–410.
16.Badertscher R, Losonsky J, Paul A, et al. Two-dimensional echocardiography for dirofilariasis in nine dogs. JAVMA 1988;193:843–846.
17.DeMadron E, Bonagura JD, O’Grady MR. Normal and paradoxical ventricular septal motion in the dog. Am J Vet Res 1985;46:1832–1841.
18.Ryan T, Petrovic O, Dillon JC, et al. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Col Cardiol 1985;5:918–927.
19.Daniels LB, Krummen DE, Blanchard DG. Echocardiography in pulmonary vascular disease. Cardiol Clin 2004;22:383–399.
20.Vieillard-Baron A, Prin S, Chergui K, et al. Echo-Doppler demonstration of acute cor pulmonale at
the bedside in the medical intensive care unit. Am J Respir Crit Care Med 2002;16:1310–1319.
21.Lopez-Candales A, Dohi K, Rakjagopalan N, et al. Right ventricular dyssynchrony in patients with pulmonary hypertension is associated with disease severity and functional class. Cardiovascular Ultrasound 2005;3.
22.Celermajor DS, Marwick TH. Echocardiographic and right heart catheterization techniques in patients with pulmonary arterial hypertension. Int J Card 2008;125:294–303.
23.Burieson K, Blanchard DG, Kuvelas T, et al. Left ventricular shape deformation and mitral valve prolapse in chronic pulmonary hypertension. Echocardiography 1994;11:537–545.
24.Hinderliter AL, Willis IV, Long W, et al. Frequency and prognostic significance of pericardial effusion in primary pulmonary hypertension. Am J Card 1999;84:481–484.
25.Mahmud E, Raisinghani A, Kermati S, et al. Dilation of the coronary sinus on echocardiogram: prevalence and significance in patients with chronic pulmonary hypertension. J Am Soc Echocard 2001;14:44–49.
26.Gunes Y, Guntekin U, Tuncer M, et al. Association of coronary sinus diameter with pulmonary hypertension. Echocardiography 2008;25:935–940.
27.McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Card 1996;78:469–473.
28.Ribeiro A, Lindmarker P, Juhlin-Dannfelt A, et al. Echocardiography Doppler in pulmonary embolism: right ventricular function as a predictor of mortality rate. Am Heart J 1997;134:479–487.
29.Capan LM, Miller SM. Monitoring for suspected pulmonary embolism. Anesthesiology Clinics of North America 2001;19:673–703.
30.Ahmed SN, Syed FM, Porembka DT. Echocardiographic evaluation of hemodynamic parameters. Crit Care Med 2007;35 Suppl:S323–329.
31.Forfia PR, Fisher MR, Mathai SC, et al. Tricuspid annular displacement predicts survival in pulmonary hypertension. Am J Respir Crit Care Med 2006;174:1034–1041.
32.Fowles RE, Hultgren HN. Left ventricular function at high altitude examined by systolic time intervals and m-mode echocardiography. Am J Card 1983;52: 862–866.
33.Sadeghi HM, Kimura BJ, Tabibiazar R, et al. Determinants of tricuspid regurgitation in pulmonary hypertension. J Am Soc Echocard 2001;14:449.
34.Hatle L, Angelsen B. Doppler Ultrasound in Cardiology. Physical Principles and Clinical Applications. 2nd ed. Philadelphia: Lea and Febiger, 1985.
35.Uehara Y. An attempt to estimate the pulmonary artery pressure in dogs by means of pulsed Doppler echocardiography. J Vet Med Sci 1993;55:307–312.
36.Hagio M. Assessment of the pathological condition of congenital heart disease: morphological and functional diagnosis by combined echocardiography. Jpn J Vet Sci 1990;43:119–129.
37.Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure among echocardiographically normal subjects. Circ 1984;70:657–662.
38.Kitabatake A, Inoue M, Asao M, et al. Noninvasive evaluation of pulmonary hypertension by a pulsed Doppler technique. Circ 1983;68:302–309.
39.Dabestani A, Mahan G, Gardin JM, et al. Evaluation of pulmonary artery pressure and resistance by pulsed Doppler echocardiography. Am J Card 1987;59:662–668.
40.Isobe M, Yazaki Y, Takaku F, et al. Prediction of pulmonary arterial pressure in adults by pulsed Doppler echocardiography. Am J Card 1986;57:316–321.
41.Sager R, Saggar R, Aboulhosn J, et al. Diagnosis and hemodynamic assessment of pulmonary arterial hypertension. Seminars in Respiratory and Critical Care Medicine 2009;30:399–410.
42.Davidson WR, Fee EC. Influence of aging on pulmonary hemodynamics in a population free of coronary artery disease. Am J Card 1990;65:1454–1458.
43.Bossone E, Rubenfire M, Bach DS, et al. Range of tricuspid regurgitant velocity at rest and during exercise in normal adult men: implications for the diagnosis of pulmonary hypertension. J Am Col Cardiol 1999;33: 1662–1666.
44.McQuillan BM, Picard MH, Leavitt M, et al. Clinical correlates and reference intervals for pulmonary artery systolic pressure among clinically normal subjects. Circ 2001;104:2797–2802.
45.De Divitiis O, Fazio S, Petitto M, et al. Obesity and cardiac function. Circ 1981;64:477–482.
46.Abbas AE, Fortuin FD, Schiller NB, et al. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Col Cardiol 2003;2003:1021–1027.
47.Ulett KB, Marwick TH. Incorporation of pulmonary vascular resistance measurement into standard echocardiography: implications for assessment of pulmonary hypertension. Echocardiography 2007;24:1020–1022.
48.Selimovic N, Rundqvist B, Berg et al. Assessment of pulmonary vascular resistance by Doppler echocardiography in patients with pulmonary arterial hypertension. J Heart Lung Transplant 2007;26:927–934.
49.Oyama MA, Sisson DD, Bulmer BJ, et al. Echocardiographic estimation of mean left atrial pressure in a canine model of acute mitral valve insufficiency. Journal of Veterinary Internal Medicine 2004;18:667–672.
50.Martin-Duran R, Larman M, Trugeda A, et al. Comparison of Doppler-determined elevated arterial pressure with pressure measured at cardiac catheterization. Am J Card 1986;57:859–863.
51.Tahara M, Tanaka H, Nakao S, et al. Hemodynamic determinants of pulmonary valve motion during systole in experimental pulmonary hypertension. Circ 1981;64: 1249–1255.
52.Mahmud E, Raisinghani A, Hassankhani A, et al. Correlation of left ventricular diastolic filling characteristics with right ventricular overload and pulmonary artery pressure in chronic thromboembolic pulmonary hypertension. J Am Col Cardiol 2002;40:318–324.
53.Wu DK, Hsiao SH, Lin SK, et al. Main pulmonary arterial distensibility: different presentation between chronic pulmonary hypertension and acute pulmonary embolism. Circ 2008;72.
54.Hsiao S-H, Wang W-C, Yang S-H, et al. Myocardial tissue doppler-based indexes to distinguish right ventricular volume overload from right ventricular pressure overload. Am J Cardiol 2008;101:536–541.
55.Miller DB, Farah MG, Liner A, et al. The relation between quantitative right ventricular ejection fraction and indices of tricuspid annular motion and myocardial performance. J Am Soc Echocard 2004;17:443–447.
56.Willens HJ, Chirinos JA, Gomez-Marin O, et al. Noninvasive differentiation of pulmonary arterial and venous hypertension using conventional and Doppler tissue imaging echocardiography. J Am Soc Echocard 2008;2008:715–719.
57.Chetboul V, Lefebvre HP, Pinhas C, et al. Spontaneous feline hypertension: clinical and echocardiographic abnormalities, and survival rate. J Vet Int Med 2003;17:89–95.
58.Littman MP. Spontaneous hypertension in 24 cats. J Vet Int Med 1994;8:79–86.
59.Snyder P. Canne hypertensive disease. Comp Cont Ed Prac Vet 1992;14:E17–23.
60.Remillard R, Ross J, Eddy J. Variance of indirect blood pressure measurements and prevalence of hypertension in clinically normal dogs. Am J Vet Res 1991;52:561–565.
61.Dukes J. Hypertension: a review of the mechanisms, manifestations and management. J Sm Anim Prac 1992;33:119–129.
62.Sparkes AH, Barnett KC, Dunn KA, et al. Inter and intraindividual variation in Doppler ultrasonic indirect blood pressure measurement in healthy cats. J Vet Int Med 1999;13:314–318.
63.Sennello KA, Schulman RL, Prosek R, et al. Systolic blood pressure in cats with diabetes mellitus. JAVMA 2003;223:198–201.
64.Nelson O, Reidesel E, Ware W, et al. Echocardiographic and radiographic changes associated with systemic hypertension in cats. Journal of Veterinary Internal Medicine 2002;16:418–425.
65.Kobayashi D, Peterson M, Graves T, et al. Hypertension in cats with chronic renal failure or hyperthyroidism. J Vet Int Med 1990;4:58–62.
66.Mahoney L, Brody M. A method for indirect recording of arterial pressure in conscious cats. J Pharm Meth 1978;1:61–66.
67.Klevans L, Hirkaler G, Kovacs J. Indirect blood pressure determination by Doppler technique in renal hypertensive cats. Am J Physiol 1979;237:H720–H723.
68.Grandi A, Venco A, Sessa F, et al. Determinants of left ventricular function before and after regression of myocardial hypertrophy in hypertension. Am J Hypertens 1993;6:708–712.
69.Karpov R, Tkachenko O, Trissvetova E, et al. Evaluation of cardiac performance in hypertension. Am J Hyper 1992;5:190S–145S.
70.Wicker P, Roudaut R, Haissaguere M, et al. Prevalence and significance of asymmetric septal hypertrophy in hypertension: an echocardiographic and clinical study. Eur Heart J suppl G 1983;4:1–
71.Morioka S, Simon G. Echocardiographic evidence for early left ventricular hypertrophy in dogs with renal hypertension. Am J Card 1982;49:1890–1895.
72.Lesser M, Fox P, Bond B. Non-invasive blood pressure evaluation in cats with left ventricular hypertrophic diseases. J Vet Int Med 1990;4:117.
73.Bovée K, Douglas P. Abnormal left ventricular shape and function in hypertensive dogs. J Vet Int Med 1990;4: 117.
74.Devereaux R, De Simone G, Ganau A, et al. Left ventricular hypertrophy and hypertension. Clin Exper Hyperten 1993;15:1025–1032.
75.Henik RA, Stepien RL, Bortnowski HB. Spectrum of M-mode echocardiographic abnormalities in
75cats with systemic hypertension. J Am Anim Hosp Assoc 2004;40:359–363.
76.Snyder PS, Sadek D, Jones GL. Effect of amlodipine on echocardiographic variables in cats with systemic hypertension. J Vet Int Med 2001;16:418–425.
77.Wang M, Yip GWK, Yang AYM, et al. Tissue Doppler imaging provides incremental prognostic value in systemic hypertension and left ventricular hypertrophy. J of Hypertension 2005;23:183–191.
78.Shapiro L, McKenna W. Left ventricular hypertrophy. Relation of structure to diastolic function in hypertension. Br Heart J 1984;51:1890–1895.
79.Matsuno Y, Morioka S, Murakami Y, et al. Left ventricular end systolic wall stress—dimension relationship in unanesthetized dogs with perinephretic hypertension. Jpn Circ J 1988;52:1370–1376.
80.Morioka S, Simon G, Cohn J. Echocardiographic assessment of left ventricular hypertrophy in dogs with renal hypertension. Jpn Circ J 1982;46:143–150.
81.Rosenthal J. Systolic and diastolic cardiac function in hypertension. J Cardiovasc Pharm 1992;19:S112–S115.
82.Troy A, Chakko S, Gash A, et al. Left ventricular function in systemic hypertension. J Cardiovasc Ultras 1983;2: 251–257.
83.Bella JN, Wachtell K, Boman K, et al. Relation of left ventricular geometry and function to aortic root dilatation in patients with systemic hypertension and left ventricular hypertrophy. Am J Card 2002;89:337–341.
84.de Simone G, Greco R, Mureddu G, et al. Relation of left ventricular diastolic properties to systolic function in arterial hypertension. Circ 1999;101:152–157.
85.Aeschbacher BC, Hutter D, Fuhrer J, et al. Diastolic dysfunction precedes myocardial hypertrophy in the development of hypertension. Am J Hyper 2000;14: 106–113.
86.Bogaty P, Mure P, Dumesnil JG. New insights into diastolic dysfunction as the cause of acute left sided failure associated with systemic hypertension and/or coronary artery disease. Am J Card 2002;89:341–345.
87.Wachtell K, Smith G, Gerdts E, et al. Left ventricular filling patterns inpatients with systemic hypertension and left ventricular hypertrophy (The Life Study). Am J Card 2000;85:466–472.
88.Tou SP, Adin DB, Estrada AH. Echocardiographic estimation of systemic systolic blood pressure in dogs with mild mitral regurgitation. J Vet Intern Med 2006;20: 1127–1131.
89.Nicolle A, Sampedrano CC, Fontaine JJ, et al. Longitudinal left ventricular myocardial dysfunction assessed by 2D colour tissue Doppler imaging in a dog with systemic hypertension and severe arteriosclerosis. 2004:83–87.
90.Poulsen SH, Anderson NH, Ivarson PI, et al. Doppler tissue imaging reveals systolic dysfunction in patients with hypertension and apparent isolated diastolic dysfunction. J Am Soc Echocard 2003;16:724–731.