Drugs

, Volume 31, Supplement 4, pp 192–201 | Cite as

Left Ventricular Hypertrophy

A Cardiovascular Risk Factor in Essential Hypertension
  • Franz H. Messerli
  • Roland Schmieder
Section 4: Diuretic Therapy and the Elderly Patient

Summary

The heart adapts to increasing afterload, such as that which occurs in arterial hypertension, with an increase in wall thickness in order to bring wall stress back to normal. As a consequence, concentric left ventricular hypertrophy ensues. Hypertension as well as advancing age has been shown to be associated with an increase in posterior wall thickness. Accordingly, the prevalence of left ventricular hypertrophy becomes very high in the elderly and may occur in more than 50% of elderly hypertensive patients. Left ventricular hypertrophy is not merely a physiological process serving to compensate for the increased afterload. The Framingham study has indicated that patients with left ventricular hypertrophy are at an increased risk of sudden death and other cardiovascular morbidity and mortality. The risk for sudden death is 5 to 6 times higher in patients with left ventricular hypertrophy than in those without, regardless of levels of arterial pressure. By Holter monitoring of these patients it has been shown that those with left ventricular hypertrophy have a prevalence of premature ventricular contractions that is 40 to 50 times higher than those patients without left ventricular hypertrophy. In addition, patients with left ventricular hypertrophy rated substantially higher with regard to Lown’s classes than those without. These data indicate that left ventricular hypertrophy is common, particularly in the elderly, and predisposes to ventricular ectopy, higher grade arrhythmias, and sudden death. Clearly, these considerations have to be taken into account when selecting antihypertensive therapy inasmuch as hypokalaemia, hypomagnesaemia, and other electrolyte shifts predisposing to ventricular arrhythmias must be scrupulously avoided.

Keywords

Left Ventricular Hypertrophy Ventricular Hypertrophy Left Ventricular Mass Premature Ventricular Contraction Ventricular Ectopy 

Résumé

Le coeur s’adapte à une post-charge croissante, comme celle qui survient dans l’hypertension artérielle, par une augmentation de l’épaisseur de la paroi pour ramener sa dilatation à la normale. En conséquence, il s’ensuit une hypertrophie ventriculaire gauche concentrique. L’hypertension, aussi bien que l’âge avancé, sont connus pour s’associer à une augmentation d’épaisseur de la paroi postérieure. Corrélativement, la prévalence de l’hypertrophie ventriculaire gauche devient très élevée chez le sujet âgé et peut survenir chez plus de 50% des sujets âgés hypertendus. L’hypertrophie ventriculaire gauche n’est pas seulement un processus physiologique servant de compensation à l’augmentation de la post-charge. L’étude de Framingham a montré que les malades en hypertrophie ventriculaire gauche présentent un risque plus grand de mort subite et d’autres processus de morbidité et de mortalité cardiovasculaires. Le risque de mort subite est 5 à 6 fois plus élevé chez les malades en hypertrophie ventriculaire gauche que chez les malades indemnes de cette pathologie. Il a été démontré par enregistrement Holter de ces malades en hypertrophie ventriculaire gauche qu’ils ont une prévalence de contractions ventriculaires prématurées de 40 à 50 fois plus élevée que les malades sans hypertrophie ventriculaire gauche. De plus, les malades en hypertrophie ventriculaire gauche se situent notablement plus haut dans la classification de Lown que ceux qui n’en ont pas. Ces données indiquent que l’hypertrophie ventriculaire gauche est fréquente, particulièrement chez le sujet âgé, et prédispose à l’ectopie ventriculaire, à des arythmies plus sévères et à la mort subite. Evidemment, on doit tenir compte de ces considérations quand on sélectionne un traitement antihypertenseur dans la mesure où l’hypokaliémie, l’hypomagnésémie et d’autres désordres électrolytiques qui prédisposent aux arythmies ventriculaire doivent être scrupuleusement évités.

Zusammenfassung

Das Herz adaptiert gegenüber einer erhöhten Nachlast, wie sie bei der arteriellen Hypertonie auftritt, mit einer Erhöhung der Wanddicke, um die Beanspruchung der Wand wieder zu normalisieren. Als eine Konsequenz erfolgt eine konzentrische links-ventrikuläre Hypertrophie. Es wurde gezeigt, daβ sowohl eine Hypertonie als auch das fortgeschrittene Alter mit einem Anstieg der posterioren Wanddicke assoziiert sind. Dem zufolge tritt eine links-ventrikuläre Hypertrophie in hohem Maβe bei den Älteren auf und kann bei mehr als 50% der älteren Hypertoniker vorkommen. Die links-ventrikuläre Hypertrophie ist nicht bloβ ein physiologischer Prozeβ, der dazu dient, die erhöhte Nachlast zu kompensieren. Die Framingham-Studie hat gezeigt, daβ Patienten mit links-ventrikulärer Hypertrophie ein erhöhtes Risiko für den plötzlichen Herztod und für andere kardiovaskuläre Morbidität und Mortalität besitzen. Das Risiko eines plötzlichen Herztodes ist 5–6mal höher bei Patienten mit links-ventrikulärer Hypertrophie als bei anderen, unabhängig von der Höhe des arteriellen Drucks. Durch Holter-Monitoring wurde nachgewiesen, daβ bei diesen Patienten mit links-ventrikulärer Hypertrophie vorzeitige ventrikuläre Kontraktionen 40–50mal häufiger sind als bei Patienten ohne eine links-ventrikuläre Hypertrophie. Auβerdem sind Patienten mit links-ventrikulärer Hypertrophie substantiell höher hinsichtlich der Lown’s-Klassen einzuordnen als jene ohne. Diese Daten zeigen an, daβ eine linksventrikuläre Hypertrophie häufig ist, insbesondere bei den Älteren und zu ventrikulären Ektopien, Arrhythmien höheren Grades und zu plötzlichem Herztod prädispioniert. Dies muβ bei der Auswahl einer antihypertensiven Therapie in Betracht gezogen werden, da eine Hypokaliämie, Hypomagnesämie und andere Elektrolytveränderungen, die zu ventrikulären Arrhythmien Anlaβ geben, peinlichst zu vermeiden sind.

Resumen

El corazón se adapta a una creciente poscarga, como la que aparece en la hipertensión arterial, aumentando el grosor de la pared con objeto de hacer volver a lo normal el esfuerzo parietal. Como consecuencia, se produce hipertrofia ventricular izquierda concéntrica. Se ha visto que la hipertensión y la edad avanzada van unidas a un aumento de grosor de la pared posterior. En consecuencia, el predominio de la hipertrofia ventricular izquierda es muy elevado en el anciano y se manifestará en más del 50% de los ancianos hipertensos. La hipertrofia ventricular izquierda no es meramente un proceso fisiológico que sirve para compensar el aumento de la poscarga. El estudio Framingham indica que los pacientes de hipertrofia ventricular izquierda corren más riesgo de muerte súbita y otras causas de morbididad y mortalidad cardiovascular. El riesgo de muerte repentina es entre cinco y seis veces mayor en los pacientes con hipertrofia ventricular izquierda que en los que no la tienen, cualesquiera que sean los nivelés de presión arterial. En el seguimiento Holter de estos sujetos se ha demostrado que los enfermos con hipertrofia ventricular izquierda muestran un predominio de contracciones ventriculares prematuras que es 40 a 50 veces mayor que el de los pacientes sin ella. Además, los casos de hipertrofia ventricular izquierda se situaron sustancialmente más arriba con respecto a las closes de Lown. Estos datos indican que la hipertrofia ventricular esfrecuente, sobre todo en el anciano, y predispone a la ectopia ventricular, a las arritmias de grado alto y a la muerte repentina. Evidentemente, hay que tener en cuenta estas consideraciones al elegir la terapéutica hipotensora: deben evitarse escrupulosamente la hipocaliemia, la hipomagnesemia y otras desviaciones electrolíticas que predisponen a las arritmias ventriculares.

Resumo

O coração se adapta às pós-cargas, tais como as que ocorrem em estado de hipertensão arterial, com um aumento na espessura da parede, a fim de trazer a tensão da parede de volta ao normal. Como consequência, ocorre hipertrofia concêntrica do ventrículo esquerdo. Demonstrou-se que tanto a hipertensão como a idade avançada estão associadas a um aumento de espessura da parede posterior. Sendo assim, a incidência de hipertrofia do ventrículo esquerdo é muito alta nos indivíduos idosos, podendo ocorrer em mais de 50% dos pacientes idosos com hipertensão. A hipertrofia do ventrículo esquerdo não é apenas um processo fisiológico para compensar a maior pós-carga. O estudo de Framingham indicou que pacientes com hipertrofia do ventriculo esquerdo correm um maior risco de morte súbita ou outra forma de morbidade ou mortalidade cardiovascular. O risco de morte súbita é 5 a 6 vezes mais alto em pacientes com hipertrofia do ventrículo esquerdo que nos que não a têm, independentemente dos níveis de pressão arterial. A aplicação de monitoria de Holter nestes pacientes revelou, nos portadores de hipertrofia do ventriculo esquerdo, que a ocorrência de contrações ventriculares prematuras é de 40 a 50 vezes mais alta que a dos não-portadores de hipertrofia do ventrículo esquerdo. Além disso, os pacientes com hipertrofia do ventrículo esquerdo, na classificação de Lown, situaram-se bem acima dos pacientes não-portadores de uma tal hipertrofia. Estes dados indicam que a hipertrofia do ventriculo esquerdo é ocorrência comum, particularmente entre pessoas idosas, predispondo à ectopia ventricular, a arritmias acentuadas e à morte súbita. Evidentemente, estas considerações têm que ser levadas em conta ao se selecionar uma terapia para hipertensão, uma vez que a hipopotassemia, a hipomagnesemia ou qualquer outra variação eletrolítica que predisponha a arritmias ventriculares deve ser escrupulosamente evitada.

Riassunto

Il cuore si adatta ad un aumento del postcarico, come quello che avviene in corso di ipertensione arteriosa, con un aumento nello spessore della parete per riportare alla norma lo stress parietale. Come conseguenza si sviluppa una ipertrofia concentrica del ventricolo sinistro. È stato dimostrato che l’ipertensione, come il progredire dell’età, sono associate ad un aumento dello spessore della parete posteriore. In accordo a ciò, la prevalenza di ipertrofia ventricolare sinistra è molto alta nell’anziano e può presentarsi in oltre il 50% degli ipertesi anziani. L’ipertrofia ventricolare sinistra non è semplicemente un processo fisiologico necessario a compensare l’aumento del postcarico. Lo studio di Framingham ha indicato che pazienti con ipertrofia ventricolare sinistra presetano un aumento del rischio di morte improvvisa e di morbilità e mortalità cardiovascolare. Il rischio di morte improvvisa è da 5 a 6 volte maggiore in pazienti con ipertrofia ventricolare sinistra rispetto a quelli che ne siano privi, indipendentemente dai livelli di pressione arteriosa. Il monitoraggio secondo Holter di questi pazienti ha dimostrato che quelli con ipertrofia ventricolare sinistra hanno una prevalenza di extrasistoli ventricolari che è 40–50 volte maggiore rispetto a quelli in cui l’ipertrofia non sia presente. Inoltre, pazienti con ipertrofia ventricolare sinistra appartengono ad una classe Lown più alta rispetto a quelli senza ipertrofia. Questi dati indicano che l’ipertrofia ventricolare sinistra è comune, specie nell’anziano, e predispone ad ectopie ventricolari, ad aritmie gravi e a morte improvvisa. Ovviamente, questi dati devono essere considerati nella scelta della terapia antiipertensiva, poichè l’ipopotassiemia, l’ipomagnesiemia e altre modificazioni elettrolitiche predisponenti le aritmie ventricolari devono essere scrupolosamente evitate.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Boreo JS, Jason M, Devereux RB. Function of the hypertrophied left ventricle at rest and exercise: hypertension and aortic stenosis. American Journal of Medicine 75 (Suppl. 3A): 34–39, 1983CrossRefGoogle Scholar
  2. Caralis PV, Materson BJ, Perez-Stable E. Potassium and diuretic-induced ventricular arrhythmias in ambulatory hypertensive patients. Mineral and Electrolyte Metabolism 10: 148–154, 1984PubMedGoogle Scholar
  3. Devereux RB, Reichek N. Repolarization abnormalities of left ventricular hypertrophy. Clinical, echocardiographic, and hemodynamic correlates. Journal of Electrocardiology 15: 47–54, 1982PubMedCrossRefGoogle Scholar
  4. Devereux RB, Savage DD, Sachs I, Laragh JH. Effect of blood pressure control of left ventricular hypertrophy and function in hypertension. Circulation 62 (Suppl. III): 111–136, 1980Google Scholar
  5. Drayer JIM, Gardin JM, Weber MA, Arronow WS. Changes in cardiac anatomy and function during therapy with alpha methyldopa: an electrocardiographic study. Current Therapeutic Research 32: 856–865, 1982aGoogle Scholar
  6. Drayer JIM, Gardin JM, Weber MA, Arronow WS. Changes in ventricular septal sickness during diuretic therapy. Clinical Pharmacology and Therapeutics 32: 283–288, 1982bPubMedCrossRefGoogle Scholar
  7. Drayer JIM, Weber MS, Gardin JM. Mediators of changes in left ventricular man during antihypertensive therapy. In Ter Keurs and Schipperheyn (Eds) Cardiac left ventricular hypertrophy, pp. 225–237, Martinus Nijhoff, The Hague, 1983Google Scholar
  8. Dunn FG, Chandraratna P, de Carvalho JGR, Basta LL, Frohlich ED. Pathophysiologic assessment of hypertensive heart disease with echocardiography. American Journal of Cardiology 39: 789–795, 1977PubMedCrossRefGoogle Scholar
  9. Dunn FG, Oigman W, Ventura HO, Messerli FH, Kobrin I, et al. Enalapril improves systemic and renal hemodynamics and allows regression of left ventricular mass in essential hypertension. American Journal of Cardiology 53: 105–108, 1984PubMedCrossRefGoogle Scholar
  10. Dreslinski GR. Identification of left ventricular hypertrophy: chest roentgenography echocardiography and electrocardiograph)’. American Journal of Medicine 75 (Suppl. 3A): 47–50, 1983PubMedCrossRefGoogle Scholar
  11. Fouad FM, Nakashima Y, Tarazi RC, Salcedo EE. Reversal of left ventricular hypertrophy in hypertensive patients treated with methyldopa. American Journal of Cardiology 49: 795–801, 1982PubMedCrossRefGoogle Scholar
  12. Fouad FM, Slominski MJ, Tarazi RC. Left ventricular diastolic function in hypertension: relation to left ventricular mass and systolic function. Journal of the American College of Cardiology 3: 1500–1506, 1984PubMedCrossRefGoogle Scholar
  13. Fouad, FM, Tarazi RC, Gallagher JH, Macintyre WJ, Cook SA. Abnormal left ventricular relaxation in hypertensive patients. Clinical Science 59: 4115–4145, 1980Google Scholar
  14. Fröhlich ED. Physiologic considerations in left ventricular hypertrophy. American Journal of Medicine 75 (Suppl. 3A): 12–18, 1983PubMedCrossRefGoogle Scholar
  15. Gaasch WH, Levine HJ, Quinones MA, Alexander JK. Left ventricular compliance: mechanisms and clinical implications. American Journal of Cardiology 38: 645–653, 1976PubMedCrossRefGoogle Scholar
  16. Gordon T, Kannel WB. Premature mortality from coronary heart disease. The Framingham study. Journal of the American Medical Association 215: 1617–1625, 1971PubMedCrossRefGoogle Scholar
  17. Granger CB, Kazimeddini MK, Smith VE, Shapiro HR, Katz AM, et al. Rapid ventricular filling in left ventricular hypertrophy: physiological hypertrophy. Journal of the American College of Cardiology 5: 862–868, 1985PubMedCrossRefGoogle Scholar
  18. Grossman W. Cardiac hypertrophy: useful adaption or pathologic process? American Journal of Medicine 69: 576–584, 1980PubMedCrossRefGoogle Scholar
  19. Grossman W, McLaurin LP, Stefadouros MA. Left ventricular stiffness associated with chronic pressure and volume overloads in man. Circulation Research 35: 793–800, 1974PubMedCrossRefGoogle Scholar
  20. Hanrath P, Mathey DG, Siegert R, Bleifeld W. Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: an echocardiographic study. American Journal of Cardiology 45: 15–21, 1980PubMedCrossRefGoogle Scholar
  21. Harrington JT, Isner JM, Kassirer JP. Our national obsession with potassium. American Journal of Medicine 73: 155–159, 1/82Google Scholar
  22. Holland OB, Nixon JV, Kuhnert LU. Diuretic induced ventricular ectopic activity. American Journal of Medicine 70: 762–768, 1981PubMedCrossRefGoogle Scholar
  23. Inouye IK, Massi, B, Loge D, Topic N, Siverstein D, et al. Abnormal left ventricular filling: an early finding in mild to moderate systemic hypertension. American Journal of Cardiology 53: 120–126, 1984PubMedCrossRefGoogle Scholar
  24. Kannel WB. Prevalence and natural history of electrocardiographic left ventricular hypertrophy. American Journal of Medicine 75 (Suppl. 3A): 4–11, 1983PubMedCrossRefGoogle Scholar
  25. Kannel WB, Castelli WP, McNamara PM, McKee PA, Feinlieb M. Role of blood pressure in the development of congestive heart failure. New England Journal of Medicine 287: 781–787, 1972PubMedCrossRefGoogle Scholar
  26. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram: prevalence, incidence, and mortality in the Framingham study. Annals of Internal Medicine 71: 89–105, 1969PubMedGoogle Scholar
  27. Kaplan NM. Our appropriate concern about hypokalemia. American Journal of Medicine 77: 1–4, 1984PubMedCrossRefGoogle Scholar
  28. Linzbach AJ. Hypertrophy, hyperplasia and structural dilation of the human heart. Advances in Cardiology 18: 1–14, 1976PubMedGoogle Scholar
  29. Marcus ML, Koyanagi S, Harrison DG, Doty DB, Hiratzka LF, et al. Abnormalities in the coronary circulation that occur as a consequence of cardiac hypertrophy. American Journal of Medicine 75 (Suppl. 3A): 62–66, 1983PubMedCrossRefGoogle Scholar
  30. Marcus ML, Mueller TM, Gascho JA, Derber RE. Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation. American Journal of Cardiology 44: 1023–1028, 1979PubMedCrossRefGoogle Scholar
  31. Messerli FH. Clinical determinants and consequences of left ventricular hypertrophy. American Journal of Medicine 75 (Suppl. 3A): 51–56, 1983aPubMedCrossRefGoogle Scholar
  32. Messerli FH. Determinants and modulators of left ventricular structure. In Ter Keurs and Schipperheyn (Eds) Cardiac left ventricular hypertrophy, pp. 39–50, Martinus Nijhoff, The Hague, 1983bGoogle Scholar
  33. Messerli FH and Devereux RB. Introduction: left ventricular hypertrophy —good or evil. American Journal of Medicine 75 (Suppl. 3A): 1–3, 1983PubMedCrossRefGoogle Scholar
  34. Messerli FH, Glade LB, Ventura HO, Dreslinski GR, Suarez DH, et al. Diurnal variations of cardiac rhythm, arterial pressure and urinary catecholamines in borderline and established essential hypertension. American Heart Journal 104: 109–114, 1982PubMedCrossRefGoogle Scholar
  35. Messerli FH, Sundgaard-Riise K, Reisin E, Dreslinski GR, Dunn FG, et al. Disparate cardiovascular effects of obesity and arterial hypertension. American Journal of Medicine 74: 808–812, 1983aPubMedCrossRefGoogle Scholar
  36. Messerli FH, Sungaard-Riise K, Reisin ED, Dreslinski GR, Ventura HO, et al. Dimorphic cardiac adaptation to obesity and arterial hypertension. Annals of Internal Medicine 99: 757–761, 1983bPubMedGoogle Scholar
  37. Messerli FH, Ventura HO, Elizardi DJ, Dunn FG, Fröhlich ED. Hypertension and sudden death: increased ventricular ectopic activity in left ventricular hypertrophy. American Journal of Medicine 77: 18–22, 1984PubMedCrossRefGoogle Scholar
  38. Opherk D, Weihe E, Zebe H, Mall G, Mehmel HC, et al. Reduced coronary reserve and ultrastructural changes of the myocardium in patients with angina pectoris, arterial hypertension and normal coronary arteries. In Strauer (Ed.) The Heart in Hypertension, pp 208–220, Springer-Verlag, Berlin, 1981Google Scholar
  39. Osier W. The Principle and the Practice of Medicine, D. Appleton & Co., New York, 1892Google Scholar
  40. Pandis IP, Kotier MN, Ren JF, Mintz GS, Ross J, et al. Development and regression of left ventricular hypertrophy. Journal of the American College of Cardiology 3: 1309–1320, 1984CrossRefGoogle Scholar
  41. Reicheck N. Echocardiographic assessment of left ventricular structure and function in hypertension. American Journal of Medicine 75 (Suppl 3A): 19–25, 1983CrossRefGoogle Scholar
  42. Reicheck N, Franklin BB, Chandler T, Muhammad A, Plappert T, et al. Reversal of left ventricular hypertrophy by antihypertensive therapy. European Heart Journal 3 (Suppl. A): 165–169, 1982Google Scholar
  43. Roberts JT, Wearn JT. Quantitative changes in the capillarymuscle relationship in human hearts during normal growth and hypertrophy. American Heart Journal 21: 617–633, 1941CrossRefGoogle Scholar
  44. Robertson WB, Strong JB. Atherosclerosis in persons with hypertension and diabetes mellitus. Laboratory Investigation 18: 538–551, 1968PubMedGoogle Scholar
  45. Rowlands DB, Glovert DR, Ireland MA, McLeay RA, Stallard TJ, et al. Assessment of left ventricular mass and its response to antihypertensive treatment. Lancet 1: 467–470, 1982PubMedCrossRefGoogle Scholar
  46. Savage DD, Drayer JIM, Henry WL, Mathews EC, Ware JH, et al. Echocardiographic assessment of cardiac anatomy and function in hypertensive patients. Circulation 59: 623–632, 1979PubMedCrossRefGoogle Scholar
  47. Savage DD, Graffison RJ, Capell WP. Factors associated with ventricular dysrhythmias identified by electrocardiographic monitoring (Abstract). American Heart Association Council on Cardiovascular Epidemiology Newsletter, 1983Google Scholar
  48. Schatzkin A, Cupples LA, Heeren T, Morelock S, Mucatel M, et al. The epidemiology of sudden unexpected death: risk factors for man and woman in the Framingham Heart Study. American Heart Journal 107: 1300–1306, 1984PubMedCrossRefGoogle Scholar
  49. Smith VE, Schulmann P, Karimeddini MK, White WB, Meeran MK, et al. Rapid ventricular hypertrophy: II. Pathologic hypertrophy. Journal of the American College of Cardiology 5: 869–874, 1985PubMedCrossRefGoogle Scholar
  50. Sokolow M, Perloff D. The prognosis of essential hypertension treated conservatively. Circulation 23: 697–713, 1961CrossRefGoogle Scholar
  51. Strauer BE. Hypertensive Heart Disease, Springer-Verlag, New York, 1980CrossRefGoogle Scholar
  52. Tarazi RC. Regression of left ventricular hypertrophy by medical treatment: present status and possible implications. American Journal of Medicine 75 (Suppl. 3A): 80–86, 1983PubMedCrossRefGoogle Scholar
  53. Tarazi RC, Ferrario CM, Dustan HP. The heart in hypertension. In Genest et al. (Eds) Hypertension: physiopathology and treatment, pp. 738–755, McGraw-Hill, New York, 1977Google Scholar
  54. Topol EJ, Traill DA, Fortuin WJ. Hypertensive hypertrophic cardiomyopathy of the elderly. New England Journal of Medicine 312: 277–283, 1985PubMedCrossRefGoogle Scholar
  55. Wicker P, Tarazi RC. Coronary blood flow in left ventricular hypertrophy: a review of experimental data. European Heart Journal 3 (Suppl. A): 111–118, 1982PubMedGoogle Scholar

Copyright information

© ADIS Press Limited 1986

Authors and Affiliations

  • Franz H. Messerli
    • 1
  • Roland Schmieder
    • 1
  1. 1.Department of Internal Medicine, Section on Hypertensive DiseasesOchsner Clinic and Alton Ochsner Medical FoundationNew OrleansUSA

Personalised recommendations