Reversal of left ventricular hypertrophy in hypertensive patients treated with methyldopa

Fouad, Fetnat M.; Nakashima, Yoshiyuki; Tarazi, Robert C.; Salcedo, Ernesto E.

doi:10.1016/0002-9149(82)91961-0

Cited by 228 publications

(40 citation statements)

References 26 publications

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“…Discrepancies between LVW and blood pressure levels have been reported in humans 29 " 31 and in spontaneously hypertensive rats, 3 2 " suggesting that factors other than tension are involved in modulating the reversal of hypertensive left ventricular hypertrophy. 33 -33 In the present animal model (two-kidney, one clip Goldblart model), the ventricular hypertrophy was predominantly influenced by the pressure rate.…”

Section: Discussionmentioning

confidence: 99%

Diltiazem and left ventricular hypertrophy in renovascular hypertensive rats.

1988

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SUMMARY The effects of diltiazem treatment (40-50 mg/kg/day orally for 8 weeks) of left ventricular hypertrophy on systemic and coronary hemodynamics and mechanical cardiac performance were investigated in renovascular hypertensive rats (Goldblatt, two-kidney, one clip). Systemic and coronary hemodynamics were determined by using radioactive microspheres in conscious, unrestrained rats. Mechanical performance was measured on isolated papillary muscle from the same animal. Nine treated hypertensive rats were compared with control groups: 12 untreated hypertensive and nine sham-operated rats. Diltiazem treatment led to an effective but incomplete control of blood pressure (from 208 ± 5 mm Hg in the untreated hypertensive group to 155 ± 3 mm Hg in the treated hypertensive group; p < 0.01) associated with a significant but incomplete decrease of the left ventricular mass (from 3.10 ± 0.19 mg/g in untreated hypertensive rats to 2.35 ± 0.04 mg/g in treated hypertensive rats; p < 0.01). A close correlation was found between left ventricular mass and systolic blood pressure in untreated, treated, and pooled groups (r = 0.84, p < 0.001, n = 30). The left ventricular weight to systolic blood pressure ratio was equivalent in all three groups, so that the reduction of left ventricular mass in diltiazem-treated rats was commensurate with the reduction of blood pressure. At rest, treated hypertensive rats showed a rise in cardiac output (426 ± 12 vs 298 ± 22 ml/min/kg in sham-operated rats; p < 0.001) and in coronary blood flow (598 ± 17 vs 453 ± 19 ml/min/100 g; p < 0.05) related to the decrease in total peripheral resistance and in total left ventricular coronary resistance. A reversal of impaired myocardial mechanical parameters toward control values was observed except for time to half-maximal relaxation (92 ± 2 msec in the treated group vs 79 ± 5 msec in sham-operated rats) and time to peak force. Our results demonstrate that even incomplete control of blood pressure with diltiazem is associated with significant but partial reduction of left ventricular mass and improvement of mechanical function. (Hypertension 11: 495-501, 1988) 6 " 8 However, these drugs exhibit substantial differences in their antihypertensive potency, site of action, and degree of sympathetic stimulation. The 1,4-dihydropyridines are very potent antihypertensive drugs, with a proven ability to lower blood pressure

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Section: Discussionmentioning

confidence: 99%

Diltiazem and left ventricular hypertrophy in renovascular hypertensive rats.

1988

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“…Secondly, most of the centers demonstrated either a lack of or a relatively poor correlation between the degree of blood pressure control and the regression of left ventricular hypertrophy. 5 " 9 The correlation between mass and pressure reportedly improved by utilizing averages of 24-hour blood pressure recordings rather than casual blood pressure levels, but even then, the index of determina-tion reached only 36% at best. l0 Finally, reversal of left ventricular hypertrophy did not occur equally in all individuals treated with the same medication.…”

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confidence: 99%

Echocardiographic studies of regression of left ventricular hypertrophy in hypertension.

Fouad‐Tarazi¹,

Liebson²

1987

Hypertension

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SUMMARY The availability of echocardiography has allowed direct determinations of left ventricular wall thickness and calculation of left ventricular mass. As a result, the past decade has witnessed a remarkable evolution in our understanding of structural changes in the heart. Moreover, cardiac hypertrophy was found to be reversible by some forms of therapy. In general, reduction of left ventricular mass became evident after 8 to 12 weeks of antihypertensive therapy. Sympatholytics (including methyldopa and reserpine), converting enzyme inhibitors (captopril and enalapril), and calcium entry blockers led to significant regression of left ventricular hypertrophy. On the other hand, arteriolar vasodilators (hydralazine, trimazosin, and minoxidil) were not associated with regression of hypertrophy despite adequate blood pressure control. Finally, data regarding diuretics and /3-blockers are controversial. These differences in results among various antihypertensive drugs reflect the multiplicity of factors modulating left ventricular hypertrophy. T HE past decade has witnessed a remarkable evolution in our understanding of structural changes in the heart and arterial system in hypertension. Not only was cardiac hypertrophy found to occur much earlier in hypertension than previously thought, 1 but it was also clearly demonstrated to be reversible by some forms of therapy within a relatively short period of time.2 This advancement was made possible by the availability of echocardiographic techniques that allowed direct determinations of left ventricular wall thickness and calculation of left ventricular mass. 3 The measurements were shown to be reliable and reproducible over time with adherence to such adequate safeguards as double blind readings, strict application of reading criteria, and use of internal checking measures. 4 The reversibility of left ventricular hypertrophy in humans has been repeatedly demonstrated by many centers.4 " 7 In general, reduction of left ventricular mass became evident after at least 8 to 12 weeks of antihypertensive therapy, 2 ' 5 ' 6 but the ability to induce this regression varied markedly among otherwise equipotent antihypertensive agents. Secondly, most of the centers demonstrated either a lack of or a relatively poor correlation between the degree of blood pressure control and the regression of left ventricular hypertrophy.5 " 9 The correlation between mass and pressure reportedly improved by utilizing averages of 24-hour blood pressure recordings rather than casual blood pressure levels, but even then, the index of determina- Methodological ConsiderationsDifferences in methods may partially account for the diversity of the results among centers. These differences include: age and sex distribution, previous treatment with antihypertensive agents, modes of assessment of hypertrophy by echocardiographic techniques, degree of hypertrophy present at the beginning of the study, reproducibility of results, duration of therapy, presence of control groups, and patient compliance.No sign...

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“…29 Echocardiographic tracings were coded and read blind and in random order by two expert observers blinded to the protocol. End-diastolic measurements of IVST, left ventricular internal dimension (LVID), and posterior wall thickness (PWT) were made according to the Penn convention protocol to measure LVM.11 This was calculated by the simple and anatomically validated formula LVM = 1.04 ((IVST + LVID + PWT)3 -LVID3) -13.6.…”

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confidence: 99%