Abstract 694: More Extensive Left Ventricular Hypertrophy in Transthyretin-Type Cardiac Amyloidosis as Compared to Primary Light-Chain Cardiac Amyloidosis

Background : Cardiac amyloidosis is generally described as a disease with left ventricular (LV) wall thickening, but data supporting LV morphologic differences between types of amyloidosis are lacking. We sought to examine LV morphologic differences between patients with light chain (AL) and transthyretin (TTR)-type amyloidosis with cardiac involvement using volumetric cardiovascular magnetic resonance (CMR). Methods : Patients with proven AL (n =21) and TTR amyloidosis (n =14) underwent cine CMR using standard methods. Volumetric LV mass, LV volumes, and LV mass/volume ratio were measured by an independent core lab blinded to all patient data, using a contiguous short-axis stack of images covering the left ventricle. Results : Both groups demonstrated a male predominance (TTR 86%, AL 67%) with patients in the TTR group older than AL group (74±8yr vs 61 ± 12yr p=0.002). There were no differences in the degree of heart failure symptoms in the TTR and AL groups: NHYA Class I: 4 vs 5; Class II/III: 9 vs 15; Class IV: 0 vs 1, respectively (p=0.68). The maximum anteroseptal thickness was greater in the TTR group (17.9 ± 3.6mm vs. 14.1 ± 3.3mm; p<0.001). Left ventricular end-diastolic mass was also greater in TTR compared to AL amyloid (236 ± 63g vs. 186 ± 61 g; p=0.02) with no significant difference in LV end-diastolic volume (TTR: 154 ± 32 ml vs. 155 ± 45 ml; p=0.89). The LV mass to volume ratio for TTR amyloidosis was significantly greater than the AL group (1.58 ± 0.5 vs. 1.24 ± 0.4; p=0.02). Conclusions : These data demonstrate that LV morphology differs between TTR and AL cardiac amyloidosis, with increased wall thickness and mass in TTR despite similar baseline symptoms and clinical characteristics. Given the reported more aggressive course of AL vs. TTR cardiac amyloidosis, the clinical significance of these findings needs to be further evaluated.

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Differences in the characteristics and contemporary cardiac outcomes of patients with light-chain versus transthyretin cardiac amyloidosis

PLoS ONE ◽

10.1371/journal.pone.0255487 ◽

2021 ◽

Vol 16 (8) ◽

pp. e0255487

Author(s):

Osnat Itzhaki Ben Zadok ◽

Mordehay Vaturi ◽

Iuliana Vaxman ◽

Zaza Iakobishvili ◽

Noa Rhurman-Shahar ◽

...

Keyword(s):

Heart Failure ◽

Light Chain ◽

Cardiac Amyloidosis ◽

Clinical Laboratory ◽

Left Ventricular ◽

Male Predominance ◽

Cardiac Outcomes ◽

Lv Mass ◽

Artery Disease

Aims To compare the baseline cardiovascular characteristics of immunoglobulin light-chain (AL) and amyloid transthyretin (ATTR) cardiac amyloidosis (CA) and to investigate patients’ contemporary cardiac outcomes. Methods Single-center analysis of clinical, laboratory, echocardiographic and cardiac magnetic resonance imaging (CMRi) characteristics of AL and ATTR-CA patients’ cohort (years 2013–2020). Results Included were 67 CA patients of whom 31 (46%) had AL-CA and 36 (54%) had ATTR-CA. Patients with ATTR-CA versus AL-CA were older (80 (IQR 70, 85) years versus 65 (IQR 60, 71) years, respectively, p<0.001) with male predominance (p = 0.038). Co-morbidities in ATTR-CA patients more frequently included diabetes mellitus (19% versus 3.0%, respectively, p = 0.060) and coronary artery disease (39% versus 10%, respectively, p = 0.010). By echocardiography, patients with ATTR-CA versus AL-CA had a trend to worse left ventricular (LV) ejection function (50 (IQR 40, 55)% versus 60 (IQR 45, 60)%, respectively, p = 0.051), yet comparable LV diastolic function. By CMRi, left atrial area (31 (IQR 27, 36)cm2 vs. 27 (IQR 23, 30)cm2, respectively, p = 0.015) and LV mass index (109 (IQR 96, 130)grams/m2 vs. 82 (IQR 72, 98)grams/m2, respectively, p = 0.011) were increased in patients with ATTR-CA versus AL-CA. Nevertheless, during follow-up (median 20 (IQR 10, 38) months), patients with AL-CA were more frequently admitted with heart failure exacerbations (HR 2.87 (95% CI 1.42, 5.81), p = 0.003) and demonstrated increased mortality (HR 2.51 (95%CI 1.19, 5.28), p = 0.015). Conclusion Despite the various similarities of AL-CA and ATTR-CA, these diseases have distinct baseline cardiovascular profiles and different heart failure course, thus merit tailored-cardiac management.

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Effect of endurance training on cardiac morphology in Alaskan sled dogs

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.4.1368 ◽

1998 ◽

Vol 85 (4) ◽

pp. 1368-1375 ◽

Cited By ~ 41

Author(s):

R. L. Stepien ◽

K. W. Hinchcliff ◽

P. D. Constable ◽

J. Olson

Keyword(s):

Endurance Training ◽

Morphological Changes ◽

Left Ventricular ◽

Volume Index ◽

Heart Weight ◽

Wall Thickening ◽

Cardiac Morphology ◽

End Diastolic Volume ◽

Sled Dogs ◽

Lv Mass

The cardiac morphology of 77 conscious Alaskan sled dogs before and after 5 mo of endurance training (20 km/day team pulling a sled and musher) was studied using two-dimensional and M-mode echocardiography. Subgroups included dogs with at least one season of previous training (“veterans”) and dogs undergoing their first season of training (“rookies”). Training resulted in a significant ( P< 0.05) decrease in resting heart rate (−15%) and significant increases in interventricular septal thickness (systole, 15%; diastole, 13%), left ventricular (LV) internal dimension in diastole (LVIDd, 4%), LV free wall thickness in systole (9%) and diastole (LVWd, 9%), and left atrial diameter (5%) in all dogs, but the increase in LVWd was greater in rookies (16%) than in veterans (7%). Training increased end-diastolic volume index (8%), LV mass index (24%), and heart weight index (24%) and decreased the LVIDd-to-LVWd ratio (−6%) but did not alter cardiac index. We conclude that increased LV mass attributable to LV dilation and hypertrophy is associated with endurance training in Alaskan sled dogs. Disproportionate LV wall thickening accompanying LV dilation suggests that cardiac morphological changes are due to volume and pressure loading. These training-induced changes are similar to those documented in human athletes undergoing combined isometric and isotonic training and differ from studies of dogs trained on treadmills.

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Abstract 17388: Cardiac MRI Derived Forward Stroke Energy is a Better Index of Left Ventricular Pump Function over Ejection Fraction in Mitral Regurgitation

Circulation ◽

10.1161/circ.132.suppl_3.17388 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Kanika Kalra ◽

Muralidhar Padala

Keyword(s):

Mitral Regurgitation ◽

Ejection Fraction ◽

Left Ventricular ◽

Wall Thickening ◽

Ventricular Contraction ◽

Plane Flow ◽

Systolic Volume ◽

Forward Stroke ◽

End Diastolic Volume ◽

Significant Difference

Introduction: Mitral regurgitation (MR) into the low impedance left atrium (LA) enables a pop off valve effect and enables a false low end-diastolic volume and increased ejection fraction (EF). EF in these patients seems falsely high even though their ventricular contraction seems impaired, thus better indices that represent ventricular contraction are required in this lesion. Hypothesis: In this study we sought to investigate if forward stroke energy (FSE), which represents the forward kinetic energy of the blood through the aortic valve is a better indicator of ventricular contraction than EF. Methods: Phase-contrast MRI was performed in patients with MR (n=63; Mild MR =23; Moderate-severe MR=40), at the aortic and mitral valve planes, to compute the transvalvular through-plane flow. EF was measured as ((end-diastolic volume- end systolic volume)/end-diastolic volume), and FSE as (forward aortic stroke volume X mean arterial pressure). LV contractility was computed as the dynamic myocardial wall thickening over the cardiac cycle. Results: Regional peak wall thickening was significantly reduced in the moderate-severe MR groups - equatorial sector (5.9±0.6mm vs. 4.3±0.4mm, p=0.02) and apical sector (6.4±0.5mm vs. 4.5±0.3mm, p=0.003), indicating LV dysfunction with higher MR severity. EF did not capture this difference in LV contraction between the groups (50.1±3.7% vs. 48.3±3.2%, p=0.72). However, FSE demonstrated a significant difference between the two groups and a significant negative correlation (6527±483 mmHg.mL vs. 4895±282 mmHg.mL, p=0.002, r(MRfraction)=-0.42, p=0.0007). Conclusions: Forward stroke energy may better capture reduced myocardial contractility in the setting of MR, than EF - the current clinical gold standard.

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566 Transthyretin and light-chain cardiac amyloidosis: clinical characteristics, echocardiographic findings, and outcomes of a large cohort of patients in Northern Italy

European Heart Journal Supplements ◽

10.1093/eurheartj/suab142.055 ◽

2021 ◽

Vol 23 (Supplement_G) ◽

Author(s):

Maria Grazia De Angelis ◽

Daniela Tomasoni ◽

Edoardo Pancaldi ◽

Elisa Pezzola ◽

Nicola Saccani ◽

...

Keyword(s):

Light Chain ◽

Cardiac Amyloidosis ◽

Global Longitudinal Strain ◽

Left Ventricular ◽

Northern Italy ◽

Volume Index ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction ◽

Significant Difference ◽

Echocardiographic Findings

Abstract Aims To describe the characteristics of a cohort of patients with cardiac amyloidosis (CA) and to compare the two most common phenotypes of CA, transthyretin (ATTR) and immunoglobulin light-chain (AL). Methods and results One-hundred and eighty patients [n = 115 (64%) men, 74 ± 11 years] were retrospectively included from January 2013 to April 2021 in a single centre in Northern Italy. The majority [n = 102 (57%)] had ATTR-CA, whereas 78 patients (43%) had AL-CA. ATTR-CA patients were older (79 ± 7 vs. 66 ± 10 years, P < 0.001) and with higher prevalence of cardiovascular comorbidities, compared to those with AL-CA. ATTR-CA patients had higher N-terminal pro-B-type natriuretic peptide (Nt-proBNP) and troponin levels, and lower haemoglobin and estimated glomerular filtration rate. Echocardiographic findings suggested a more advanced stage of the disease in the ATTR-CA subgroup [left ventricular ejection fraction (LVEF), 51 ± 10% vs. 60 ± 9%; global longitudinal strain (GLS), −11 ± 3% vs. −13 ± 4%; peak systolic wall motion velocity, 4.9 ± 1.7 vs. 6.4 ± 1.9; left ventricular mass index (LVMI) 316 ± 133 g/m2 vs. 157 ± 72 g/m2; left atrium volume index (LAVI) 48 ± 17 ml vs. 40 ± 16 ml; right ventricular diameter 31 ± 9 mm vs. 22 ± 5 mm; tricuspidal annular plane systolic excursion (TAPSE) 17 ± 5 vs. 19 ± 5; all P < 0.05). During a median follow-up of 15 (6–31) months, 68 (38%) patients died. All-cause death occurred in 31% vs. 46% patients with ATTR- and AL-CA, respectively. AL-CA was an independent predictor of mortality (adjusted hazard ratio 2.62, 95% confidence interval 1.55–4.43; P < 0.001). Other independent predictors of mortality were age, systolic blood pressure, Nt-proBNP, troponin and GLS. When cardiovascular (CV) death was considered, there was no significant difference between the two phenotypes (log rank P = 0.384). Conclusions Despite ATTR-CA patients showed worse baseline characteristics, suggesting a more advanced disease at presentation, AL-CA phenotype was associated with a higher risk of all-cause death. Of note, CV mortality was comparable between the two groups.

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Increased ACE and chymase-like activity in cardiac tissue of dogs with chronic mitral regurgitation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.269.6.h2065 ◽

1995 ◽

Vol 269 (6) ◽

pp. H2065-H2073 ◽

Cited By ~ 16

Author(s):

L. J. Dell'Italia ◽

Q. C. Meng ◽

E. Balcells ◽

I. M. Straeter-Knowlen ◽

G. H. Hankes ◽

...

Keyword(s):

Mitral Regurgitation ◽

Volume Ratio ◽

Wall Stress ◽

Left Ventricular ◽

Ang Ii ◽

End Diastolic Volume ◽

Lv Mass ◽

Ace Activity

The current study was designed to test the hypothesis that intracardiac angiotensin-converting enzyme (ACE) activity, chymase-like activity, and angiotensin (ANG) peptide levels are increased and are positively related to wall stress estimates in response to the chronic low pressure volume overload of mitral regurgitation produced by percutaneous chordal rupture in the dog. Chronic mitral regurgitation (MR) resulted in an increase in left ventricular (LV) end-diastolic volume [59 +/- 11 (SD) to 103 +/- 32 ml, P < 0.001], LV mass (96 +/- 17 to 114 +/- 23 g, P < 0.001), and a decrease in the LV mass-to-end-diastolic volume ratio (1.64 +/- 0.22 to 1.16 +/- 0.23 g/ml, P < 0.001) measured by magnetic resonance imaging. In vitro studies of heart tissue extracts demonstrated that the majority of ANG II-forming activity was from chymase-like activity rather than from ACE activity in five normal (83.5 +/- 7.5 vs. 6.04 +/- 5.2%) and seven MR hearts (86 +/- 3.9 vs. 2.6 +/- 1.7%). ACE activity (1.22 +/- 0.22 vs. 3.55 +/- 0.62 mU/g, P < 0.05) and chymase-like activity (9.42 +/- 4.64 vs. 20.60 +/- 8.41 nmol.g-1.min-1, P < 0.05) were increased in MR compared with normal hearts. ACE activity correlated with the LV mass-to-volume ratio (r = -0.93, P < 0.001) and LV diastolic wall stress ( r = 0.71, P < 0.05); however, chymase-like activity did not correlate with any hemodynamic parameter. ANG II levels were significantly higher in the midwall of the left ventricle in MR hearts than in normal controls (85 +/- 39 vs. 27 +/- 16 pg/g, P < 0.01). Our results demonstrate a positive correlation between LV diastolic wall stress and increased ACE activity with increased ANG II stores, suggesting that mechanical wall stress activated intracardiac ACE. Although chymase accounted for most ANG II formation in vitro in extracts of both normal and MR dog hearts, the significance of this enzyme in vivo remains unclear

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Effects of candesartan on left ventricular hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy

European Heart Journal ◽

10.1093/ehjci/ehaa946.3360 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

H Maqsood ◽

H.A Shakeel ◽

H.F Shoukat ◽

M.D Khan ◽

S.A.Y Shah ◽

...

Keyword(s):

Late Gadolinium Enhancement ◽

Hypertrophic Cardiomyopathy ◽

Interstitial Fibrosis ◽

Angiotensin Receptor Blockers ◽

Left Ventricular ◽

Funding Source ◽

Gadolinium Enhancement ◽

Percent Change ◽

Lv Mass ◽

Significant Difference

Abstract Introduction Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular (LV) hypertrophy in the absence of pressure overload. Manifestations of the disease include heart failure associated with diastolic dysfunction and atrial and ventricular tachyarrhythmias. Pathological features of HCM include myocyte hypertrophy, interstitial fibrosis, and myocyte disarray and are mediated by angiotensin II. Purpose This study aimed to evaluate the effects of candesartan on left ventricular (LV) hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy (HCM). Methods In double-blind fashion, 30 patients (6 women, 24 men; age: 55±11 years) with HCM were randomly assigned to receive placebo (n=13) or candesartan 50 mg twice a day (n=17) for 1 year. To measure LV mass and extent of fibrosis, cardiac magnetic resonance imaging was performed at baseline and 1 year as assessed by late gadolinium enhancement. Results There was a trend toward a significant difference in the percent change in LV mass (median: +5% with placebo vs. −5% with candesartan; p=0.06). There was a significant difference in the percent change in the extent of late gadolinium enhancement, with the placebo group experiencing a larger increase (+30±27% with placebo vs. −22±44% with candesartan; p=0.03). Conclusion Our study concludes reduction of the progression of myocardial hypertrophy and fibrosis with candesartan in patients with hypertrophic cardiomyopathy. Our study population was limited so we warrant larger trials to confirm a place for angiotensin receptor blockers in the management of patients with hypertrophic cardiomyopathy. Figure 1 Funding Acknowledgement Type of funding source: Other. Main funding source(s): Self funding

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Cardiac magnetic resonance T1 mapping allows for predicting adverse left ventricular remodeling post-reperfused st-elevation myocardial infarction

European Heart Journal ◽

10.1093/ehjci/ehaa946.1583 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

L Zhang ◽

Y.K Guo ◽

Z.G Yang ◽

M.X Yang ◽

K.Y Diao ◽

...

Keyword(s):

Myocardial Infarction ◽

T1 Mapping ◽

Ventricular Remodeling ◽

Tissue Injury ◽

Left Ventricular ◽

Funding Source ◽

Native T1 ◽

End Diastolic Volume ◽

Significant Difference ◽

Lv Remodeling

Abstract Background Cardiac magnet resonance (CMR) T1 mapping allows the quantitative characterization of the severity of tissue injury and predict functional recovery in acute myocardial infarction (AMI). Purpose The study aimed to investigate whether native T1 and ECV of infarct myocardium are influenced by microvascular obstruction (MVO) and have predictive value for adverse left ventricular (LV) remodeling post-infarction. Method A cohort of 54 patients with successfully reperfused STEMI underwent CMR imaging at a 3T scanner in AMI and 3 months post-infarction. Native T1 data was acquired using a modified Look-Locker inversion recovery (MOLLI) sequence, and ECV maps were calculated using blood sampled hematocrit. Manual regions-of-interest were drawn within the infarct myocardium to measure native T1 and ECV (native T1infarct and ECVinfarct, respectively). MVO identified as a low-intensity area within the infarct zone on LGE was eliminated. Results MVO was present in 36 patients (66.67%) in AMI. ECVinfarct in patients with MVO was different from those without (58.66±8.71% vs. 49.64±8.82%, P=0.001), while no significant difference in T1infarct was observed between patients with and without MVO (1474.7±63.5ms vs. 1495.4±98.0ms, P=0.352). ECV correlated well with the change in end-diastolic volume (all patients: r=0.564, P<0.001) and predicted LV remodeling in patients with and without MVO (rMVO absent = 0.626, P=0.005; rMVO present = 0.686, P<0.001; all patients: r=0.622, P<0.001); Native T1 was only associated with a 3-month change in LV end-diastolic volume (rMVO absent= 0.483, P=0.042) and predicted LV remodeling in patients without MVO (rMVO absent = 0.659, P=0.003). Furthermore, ECV had an association with LV remodeling (β=0.312, P=0.007) in multivariable logistic analysis. Conclusion Absolute native T1 in infarct myocardium might be affected by MVO but ECV isn't. ECV could predict LV remodeling in MI patients with and without MVO, while native T1 predict it in MI with MVO absent. Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): 1·3·5 project for disciplines of excellence, West China Hospital, Sichuan University

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Natural history and disease progression of early cardiac amyloidosis evaluated by echocardiography

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jeaa356.387 ◽

2021 ◽

Vol 22 (Supplement_1) ◽

Author(s):

O Itzhaki Ben Zadok ◽

A Eisen ◽

Y Shapira ◽

D Monakier ◽

Z Iakobishvili ◽

...

Keyword(s):

Disease Progression ◽

Wall Thickness ◽

Cardiac Amyloidosis ◽

Time Course ◽

Right Ventricular Dysfunction ◽

Disease Diagnosis ◽

Left Ventricular ◽

Funding Sources ◽

Lv Mass ◽

Echocardiographic Findings

Abstract Funding Acknowledgements Type of funding sources: None. Background Since the diagnosis of cardiac amyloidosis (CA) is often delayed, echocardiographic findings are frequently indicative of already advanced cardiomyopathy. Aims to describe early echocardiographic features in patients subsequently diagnosed with CA and to delineate disease progression. Methods Pre-amyloid diagnosis echocardiographic studies were screened for structural and functional parameters and stratified according to the pathogenetic amyloid subtype (immunoglobulin light-chain (AL) or amyloid transthyretin (ATTR)). Abnormalities were defined based on published guidelines. Results Our cohort included 75 CA patients of whom 42 (56%) were diagnosed with AL and 33 (44%) with ATTR. Forty-two patients had an earlier echocardiography exam available for review. Patients presented with increased wall thickness (1.3 (IQR 1.0, 1.5)cm) ≥3 years before the diagnosis of CA and relative wall thickness (RWT) was increased (0.47 (IQR 0.41, 0.50)) ≥7 years pre-diagnosis. Between 1 to 3 years before CA diagnosis restrictive left ventricular (LV) filling pattern was present in 19% of patients and LV ejection fraction (LVEF)≤50% was present in 21% of patients. Right ventricular dysfunction was detected concomitantly with disease diagnosis. The echocardiographic phenotype of ATTR versus AL-CA showed increased RWT (0.74 (IQR 0.62, 0.92) vs. 0.62 (IQR 0.54, 0.76), p = 0.004) and LV mass index (144 (IQR 129, 191) vs. 115 (IQR 105, 146)g/m2,p = 0.020) and reduced LVEF (50 (IQR 44, 58) vs. (60 (IQR 53, 60)%, p = 0.009) throughout the time course of CA progression, albeit survival time was similar. Conclusions Increased wall thickness and diastolic dysfunction in CA develop over a time course of several years and can be diagnosed in their earlier stages by standard echocardiography Abstract Figure. Schematic proposed timeline of CA

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Impact of Papillary Muscle Infarction on Ischemic Mitral Regurgitation Assessed by Magnetic Resonance Imaging

RöFo - Fortschritte auf dem Gebiet der Röntgenstrahlen und der bildgebenden Verfahren ◽

10.1055/s-0043-115121 ◽

2017 ◽

Vol 190 (01) ◽

pp. 42-50 ◽

Cited By ~ 1

Author(s):

Christiane Bretschneider ◽

Hannah-Klara Heinrich ◽

Achim Seeger ◽

Christof Burgstahler ◽

Stephan Miller ◽

...

Keyword(s):

Myocardial Infarction ◽

Mitral Regurgitation ◽

Left Ventricular Function ◽

Ventricular Function ◽

Papillary Muscle ◽

Left Ventricular ◽

Ischemic Mitral Regurgitation ◽

Chronic Myocardial Infarction ◽

End Diastolic Volume ◽

Significant Difference

Objective Ischemic mitral regurgitation is a predictor of heart failure resulting in increased mortality in patients with chronic myocardial infarction. It is uncertain whether the presence of papillary muscle (PM) infarction contributes to the development of mitral regurgitation in patients with chronic myocardial infarction (MI). The aim of the present study was to assess the correlation of PM infarction depicted by MRI with mitral regurgitation and left ventricular function. Methods and Materials 48 patients with chronic MI and recent MRI and echocardiography were retrospectively included. The location and extent of MI depicted by MRI were correlated with left ventricular function assessed by MRI and mitral regurgitation assessed by echocardiography. The presence, location and extent of PM infarction depicted by late gadolinium enhancement (LGE-) MRI were correlated with functional parameters and compared with patients with chronic MI but no PM involvement. Results PM infarction was found in 11 of 48 patients (23 %) using LGE-MRI. 8/11 patients (73 %) with PM infarction and 22/37 patients (59 %) without PM involvement in MI had ischemic mitral regurgitation. There was no significant difference between location, extent of MI and presence of mitral regurgitation between patients with and without PM involvement in myocardial infarction. In 4/4 patients with complete and in 4/7 patients with partial PM infarction, mitral regurgitation was present. The normalized mean left ventricular end-diastolic volume was increased in patients with ischemic mitral regurgitation. Conclusion The presence of PM infarction does not correlate with ischemic mitral regurgitation. In patients with complete PM infarction and consequent discontinuity of viable tissue in the PM-chorda-mitral valve complex, the probability of developing ischemic mitral regurgitation seems to be increased. However, the severity of mitral regurgitation is not increased compared to patients with partial or no PM infarction. Key points Citation Format

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Enalapril attenuates cardiorenal damage in nitric-oxide-deficient spontaneously hypertensive rats

Clinical Science ◽

10.1042/cs20030268 ◽

2004 ◽

Vol 106 (3) ◽

pp. 337-343 ◽

Cited By ~ 15

Author(s):

Leila M. M. PEREIRA ◽

Daniele G. BEZERRA ◽

Denise L. MACHADO ◽

Carlos A. MANDARIM-DE-LACERDA

Keyword(s):

Nitric Oxide ◽

Body Mass ◽

Structural Damage ◽

Spontaneously Hypertensive Rats ◽

Left Ventricular ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Genetic Hypertension ◽

Lv Mass ◽

Significant Difference

Stereological structural alterations of the heart and kidney were studied in four groups (n=5) of spontaneously hypertensive rats (SHRs) treated for 30 days: (i) control, (ii) NG-nitro-L-arginine methyl ester [L-NAME; nitric oxide (NO) synthesis inhibitor] alone, (iii) enalapril alone and (iv) L-NAME plus enalapril. Blood pressure (BP) was elevated significantly in NO-deficient SHRs (rats receiving L-NAME) or significantly lower in enalapril-treated SHRs. Co-administration of L-NAME and enalapril caused a 20% decrease in BP compared with untreated SHRs. NO-deficient SHRs had a decrease in body mass, but this loss of body mass was prevented efficiently in the enalapril-treated group. Enalapril treatment decreased the left ventricular (LV) mass index in SHRs, even in animals with NO synthesis blocked. NO deficiency in SHRs caused a larger decrease in the number of LV cardiomyocyte nuclei, which had a negative correlation with both LV mass index and BP. The volume-weighted glomerular volume (VWGV) separated the SHRs into two groupings: (i) control and NO-deficient SHRs, and (ii) enalapril- and L-NAME plus enalapril-treated SHRs. There was a significant difference between these two groupings, with VWGV being more than 15% smaller in the latter compared with the former grouping. The present findings reinforce the evidence that enalapril efficiently treats genetic hypertension, and demonstrate that this effect is observed even when NO synthesis is inhibited. Enalapril administration also decreases cardiac and renal structural damage caused by genetic hypertension, as well as by the interaction between genetic hypertension and NO deficiency.

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