Angiotensin-Converting Enzyme Inhibitor Therapy Affects Left Ventricular Mass in Patients With Ejection Fraction &gt;40% After Acute Myocardial Infarction

Johnson, David; Foster, Robert E.; Barillà, Francesco; Blackwell, Gerald G.; Roney, Maryann; Stanley, Alfred W.H.; Kirk, Kathy; Orr, Roger; Geest, Rob J. van der; Reiber, J. H. C.; Dell’Italia, Louis J.

doi:10.1016/s0735-1097(96)00451-2

Cited by 35 publications

(14 citation statements)

References 43 publications

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“…[1][2][3] As a result, an increasing number of patients undergoing coronary artery bypass or valve surgery are now chronically treated with angiotensin-converting enzyme inhibitors (ACEIs). Some of these patients are prone to develop hypotensive episodes during anesthesia induction and weaning from cardiopulmonary bypass.…”

Section: Resultsmentioning

confidence: 99%

Cardiovascular responses to anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors

Licker¹,

Schweizer²,

Hohn³

et al. 2000

Can J Anesth/J Can Anesth

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Purpose: To investigate the effects of chronic ACE inhibition on cardiac neural function following induction of general anesthesia in patients with underlying coronary artery disease. Method:In a prospective case-control study, heart rate variability (HRV) and baroreflex control were compared preoperatively and 30 min after anesthesia induction in patients receiving, or not, ACEI (n=16, control group and n=16, ACEI group). All patients had normal cardiac function and anesthesia consisted of a fixed dose regimen of fentanyl and midazolam. Anesthesia-related hypotension was defined by systolic blood pressure < 90 mmHg. Spectral density of HRV was calculated for low frequency and high frequency bands (LF, from 0.05 to 0.15 Hz and HF, from > 0.15 to 0.6 Hz). Baroreflex sensitivity was estimated after blood pressure changes induced by injections of phenylephrine (PHE) and nitroglycerin (NTG). Results:The HRV parameters and baroreflex sensitivity were not different between groups, during the awake and anesthesia periods. Anesthesia produced similar reduction in total HRV in the Control and ACEI groups (-93 ± 28% vs -89 ± 32%,) and in baroreflex sensitivity during NTG (-64 ± 21% vs -54 ± 17%) or PHE tests (-74 ± 25% vs -72 ± 22%). Anesthesia-related hypotension occurred in nine patients in the ACEI group (vs two controls). Although the hypertensive response to phenylephrine was greater after anesthesia in both groups, the sensitivity to phenylephrine was attenuated in those patients experiencing hypotension in the ACEI group. Conclusions: Chronic preoperative treatment with ACEIs does not influence cardiac autonomic regulation and anesthetic-induced hypotensive episodes are mainly attributed to decreased -adrenergic vasoconstrictive response.Objectif : Rechercher les effets d'une inhibition chronique de l'ECA sur la fonction neurale cardiaque à la suite de l'induction d'une anesthésie générale chez des patients qui présentent une cardiopathie ischémique sous-jacente.Méthode : Lors d'une étude prospective cas-témoins, la variabilité de la fréquence cardiaque (VFC) et le contrôle baroréflexe ont été comparés avant l'opération et 30 min après l'induction de l'anesthésie chez des patients qui reçoivent, ou non, un IECA (groupe témoin : n = 16, groupe IECA : n = 16). Tous les patients présentaient une fonction cardiaque normale et l'anesthésie comprenait un schéma posologique fixe de fentanyl et de midazolam. On a défini l'hypotension reliée à l'anesthésie comme la tension artérielle systolique < 90 mmHg. La densité spectrale de la VFC a été calculée pour des bandes de basses et de hautes fréquences (BF, de 0,05 à 0,15 Hz et HF, de > 0,15 à 0,6 Hz). La sensibilité baroréflexe a été évaluée après les changements de pression sanguine induits par les injections de phényléphrine (PHE) et de nitroglycérine (NTG).Résultats : Les paramètres de la VFC et la sensibilité baroréflexe n'ont pas présenté de différence intergroupe pendant les périodes d'éveil et d'anesthésie. L'anesthésie a produit une réduction similaire de la VFC total...

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Section: Resultsmentioning

confidence: 99%

Cardiovascular responses to anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors

Licker¹,

Schweizer²,

Hohn³

et al. 2000

Can J Anesth/J Can Anesth

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“…Biplane long-axis MRI provides an excellent appreciation of overall cardiac anatomy in a format similar that of echocardiography and thus familiar to cardiologists. Due to the possibility of multiphasic acquisitions with excellent temporal resolution, cine MRI images are also well suited for the analysis of global and regional geometry and function [2, 3, 4]. …”

Section: Introductionmentioning

confidence: 99%

“…Cardiac remodeling following infarction has been studied by echocardiography [5], contrast and radionuclide ventriculography [6, 7]and by MRI [3, 8]. Long-term left ventricular (LV) remodeling after AMI has, however, only sparsely been examined in serial MRI studies [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Serial Magnetic Resonance Imaging of Global and Regional Left Ventricular Remodeling during 1 Year after Acute Myocardial Infarction

et al. 2001

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Biplane long-axis cine MRI was performed in 51 patients 1, 13, 26, and 52 weeks after their first AMI. LV mass index (LVMI) was significantly increased 1 week after AMI (84.3 ± 16.9 vs. 68.1 ± 11.4 g/m² controls, n = 48, p < 0.001), presumably owing to edema of the infarcted myocardium. Six months after AMI, LVMI decreased to 76.5 ± 16.4 g/m², but had again augmented after 1 year (81.8 ± 17.3 g/m², p < 0.05), suggesting late, compensatory left ventricular hypertrophy. In patients treated with primary percutaneous transluminal coronary angioplasty, LVMI decreased 5% over 1 year, while LVMI increased 10% in patients receiving thrombolysis (p < 0.05). In the entire population, the global increase in LVMI 1 year after AMI seemed to reflect global cavity dilatation with unchanged thickness of the vital myocardium. In conclusion, in patients receiving contemporary treatment, LV remodeling only partially complied with the classical patho-anatomical concept.

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“…5,6 Inhibition of angiotensin-converting enzyme (ACE) or the angiotensin II type 1 receptor (AT1-R) induced regression of myocardial hypertrophy in patients with hypertension or after myocardial infarction. [7][8][9] In HCM, ACE and AT1-R gene polymorphisms have been shown to be associated with severity of hypertrophy, a high incidence of atrial fibrillation and the risk of sudden cardiac death. 10 -17 Therefore, we designed a double-blind, placebo-controlled, randomized, multicenter study to test the safety and effects of AT1-R antagonist candesartan in patients with nonobstructive HCM.…”

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confidence: 99%

The Effects of Candesartan on Left Ventricular Hypertrophy and Function in Nonobstructive Hypertrophic Cardiomyopathy

Pěnička

Gregor

Kerekes³

et al. 2009

The Journal of Molecular Diagnostics

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Hypertrophic cardiomyopathy is caused by mutations in the genes that encode sarcomeric proteins and is primarily characterized by unexplained left ventricular hypertrophy, impaired cardiac function, reduced exercise tolerance, and a relatively high incidence of sudden cardiac death, especially in the young. The extent of left ventricular hypertrophy is one of the major determinants of disease prognosis. Angiotensin II has trophic effects on the heart and plays an important role in the development of myocardial hypertrophy. Here in a double-blind, placebo-controlled, randomized study, we show that the long-term administration of the angiotensin II type 1 receptor antagonist candesartan in patients with hypertrophic cardiomyopathy was associated with the significant regression of left ventricular hypertrophy, improvement of left ventricular function, and exercise tolerance. The magnitude of the treatment effect was dependent on specific sarcomeric protein gene mutations that had the greatest responses on the carriers of ß-myosin heavy chain and cardiac myosin binding protein C gene mutations. These data indicate that modulating the role of angiotensin II in the development of hypertrophy is specific with respect to both the affected sarcomeric protein gene and the affected codon within that gene. Thus, angiotensin II type 1 receptor blockade has the potential to attenuate myocardial hypertrophy and may, therefore, provide a new treatment option to prevent sudden cardiac death in patients with hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy (HCM) is a primary cardiac disease characterized by unexplained cardiac hypertrophy and a relatively high incidence of sudden cardiac death, especially in young people.1,2 The extent of left ventricular hypertrophy is one of the major determinants of symptoms and prognosis. 3,4 Angiotensin II has trophic effects on the heart and plays an important role in the development of myocardial hypertrophy. 5,6 Inhibition of angiotensin-converting enzyme (ACE) or the angiotensin II type 1 receptor (AT1-R) induced regression of myocardial hypertrophy in patients with hypertension or after myocardial infarction. [7][8][9] In HCM, ACE and AT1-R gene polymorphisms have been shown to be associated with severity of hypertrophy, a high incidence of atrial fibrillation and the risk of sudden cardiac death. -17Therefore, we designed a double-blind, placebo-controlled, randomized, multicenter study to test the safety and effects of AT1-R antagonist candesartan in patients with nonobstructive HCM. We hypothesized that long-term use of candesartan would be associated with regression of left ventricular (LV) hypertrophy and improvement of LV function. Materials and Methods PatientsThis was a double-blind, placebo-controlled, randomized multicenter study. The study population consisted of 24 consecutive, genetically independent, adult (Ն18 years) patients (age 43 Ϯ 13 yrs; 46% males) with nonobstructive HCM, and normal ejection fraction (Ն60%) and sinus rhythm, who visited the participating in...

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Angiotensin-Converting Enzyme Inhibitor Therapy Affects Left Ventricular Mass in Patients With Ejection Fraction >40% After Acute Myocardial Infarction

Cited by 35 publications

References 43 publications

Cardiovascular responses to anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors

Cardiovascular responses to anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors

Serial Magnetic Resonance Imaging of Global and Regional Left Ventricular Remodeling during 1 Year after Acute Myocardial Infarction

The Effects of Candesartan on Left Ventricular Hypertrophy and Function in Nonobstructive Hypertrophic Cardiomyopathy

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