Increased enddiastolic wall stress precedes left ventricular hypertrophy in dilative heart failure—Use of the volume-based wall stress index

Alter, Peter; Rupp, Heinz; Stoll, Florian; Adams, Philipp; Figiel, Jens; Klose, K. J.; Rominger, Marga B.; Maisch, Bernhard

doi:10.1016/j.ijcard.2011.07.092

Cited by 54 publications

(42 citation statements)

References 38 publications

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“…For calculation of the wall stress index at enddiastole and end-systole, LV cavity and myocardial volumes were inserted as measured using CMR imaging. 18 Wall stress was obtained by multiplication of the wall stress index with pressure. Therefore, an intraventricular pressure of 16 mm Hg at end-diastole and 130 mm Hg at end-systole was assumed for approximation as previously described in detail.…”

Section: Methodsmentioning

confidence: 99%

From Heart Failure to Highly Unsaturated Fatty Acid Deficiency and Vice Versa: Bidirectional Heart and Liver Interactions

Alter

Glück

Figiel

et al. 2016

Canadian Journal of Cardiology

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Section: Methodsmentioning

confidence: 99%

From Heart Failure to Highly Unsaturated Fatty Acid Deficiency and Vice Versa: Bidirectional Heart and Liver Interactions

Alter

Glück

Figiel

et al. 2016

Canadian Journal of Cardiology

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“…5 Based on the reported LV mass and volume and using the wall stress index, it has to be assumed that LV end-diastolic and end-systolic wall stress was increased to 4.9 kPa versus 4.6 kPa (end-diastolic LV pressure assumed at 16 mm Hg, normal end-diastolic wall stress <4 kPa) and to 28.0 kPa versus 21.0 kPa (peripheral systolic pressure inserted as reported, normal endsystolic wall stress <18 kPa), respectively. 4 Because load reduction is the principal feature of heart failure treatment, it is probable that previously untreated or undertreated patients with increased LV wall stress responded to a greater degree. Thus, we suggest to calculate wall stress and evaluate the hypothesis whether increased wall stress is a causative prognostic risk factor in DCM.…”

Section: E77mentioning

confidence: 99%

“…1 We have recently shown in 502 patients with DCM that LV dilatation is correlated with increased wall stress, which precedes the development of LV hypertrophy. 4 Because the ensuing hypertrophy is still inappropriate, greater dilatation is associated with wall stress increase. Increased LV wall stress exhibits various adverse consequences, for example, an impaired autonomic tone, favoring of arrhythmias by opening of ion channels, increased oxygen consumption, and an adverse remodeling with unfavorable prognostic consequences.…”

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confidence: 99%

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Letter by Alter Regarding Article, “Myocardial Fibrosis as a Key Determinant of Left Ventricular Remodeling in Idiopathic Dilated Cardiomyopathy: A Contrast-Enhanced Cardiovascular Magnetic Study”

Alter

2013

Circ: Cardiovascular Imaging

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Late gadolinium enhancement (LGE) as assessed by MRI is a frequent finding in various cardiac diseases. While delineating postinfarct scar accurately, there are controversies on causes and consequences in dilative cardiomyopathy (DCM). The thorough study by Masci et al 1 examined absence of LGE and deduced nonexistence of myocardial fibrosis as prognostic predictor of a favorable left ventricular (LV) remodeling in 58 patients with DCM. Of note, patients' medical heart failure therapy was optimized after enrollment in the study.For interpretation of LGE, differentiation of a variety of types and forms seems to be required. In particular, the most common streakylike occurrence in DCM at the (mechanically loaded) septal midwall or at the hinge points is of major interest. It was recently shown in 300 patients with DCM that LGE correlates with increased LV wall stress.2 Studies on DCM demonstrating increased fibrosis by histology and a matching LGE pattern have been rare. Beyond a total rise of fibrosis, the degree involves a gradient that increases from epicardial to endocardial layers of transmural LV sections and from the right to the left side of the septum not matching a midwall pattern. Thus, it remains ambiguous whether there is indeed a one-to-one relation between LGE and fibrosis. Currently, emerging techniques of pre-and postcontrast T1 mapping seem to be very promising to provide further insight into tissue characterization by cardiac MRI.The question arises whether other prognostic determinants could have been involved in the study. 1 We have recently shown in 502 patients with DCM that LV dilatation is correlated with increased wall stress, which precedes the development of LV hypertrophy. 4 Because the ensuing hypertrophy is still inappropriate, greater dilatation is associated with wall stress increase. Increased LV wall stress exhibits various adverse consequences, for example, an impaired autonomic tone, favoring of arrhythmias by opening of ion channels, increased oxygen consumption, and an adverse remodeling with unfavorable prognostic consequences. Applying these findings to the referenced study, it has to be inferred that at time of enrollment LV wall stress was markedly increased in patients responding to initiation or intensification of heart failure treatment with a favorable remodeling, which is also reflected by the fact of increased N-terminal pro-brain natriuretic peptide as reported.1 Brain natriuretic peptide correlates with ventricular wall stress.5 Based on the reported LV mass and volume and using the wall stress index, it has to be assumed that LV end-diastolic and end-systolic wall stress was increased to 4.9 kPa versus 4.6 kPa (end-diastolic LV pressure assumed at 16 mm Hg, normal end-diastolic wall stress <4 kPa) and to 28.0 kPa versus 21.0 kPa (peripheral systolic pressure inserted as reported, normal endsystolic wall stress <18 kPa), respectively. 4 Because load reduction is the principal feature of heart failure treatment, it is probable that previously untreated or undertrea...

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“…On similar lines, we have shown in experimental animals that ω-3 fatty acids attenuate left ventricular (LV) dilatation, which is a major cause of heart failure progression [5] particularly when wall stress is increased [6,7,8]. Since the amount of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) administered was much higher than the daily 840 mg EPA/DHA used in post-myocardial infarction patients [9], the dose for patients with dilative heart failure remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Replacement of Reduced Highly Unsaturated Fatty Acids (HUFA Deficiency) in Dilative Heart Failure: Dosage of EPA/DHA and Variability of Adverse Peroxides and Aldehydes in Dietary Supplement Fish Oils

Rupp

Rupp²,

Alter³

et al. 2013

Cardiology

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Objectives: To explore the rationale for ω-3 fatty acids in heart failure treatment, the dosage of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) for replacing low levels of highly unsaturated fatty acids (HUFA deficiency) was examined. To judge the usefulness of various EPA/DHA preparations, their content of peroxides and aldehydes was determined. Methods: In 298 patients with dilative heart failure, the serum HUFA level was assessed by gas chromatography. In ω-3-acid ethyl esters 90 (Omacor/Lovaza, approved by the Food and Drug Administration and the European Medicines Agency) and 63 dietary supplement fish oils, oxidation products were determined by photometry. Results: Increasing serum HUFA from the lower (4.3 ± 1.0%) to the upper (9.5 ± 1.5%) tertile would be associated with an increased left ventricular (LV) ejection fraction (34.1 ± 9.9 vs. 28.3 ± 9.5%, p < 0.01) and reduced LV enddiastolic diameter (63.5 ± 7.1 vs. 66.9 ± 7.4 mm) requiring at least 2 g EPA/DHA daily. In fish oils, the peroxide and alkenal level varied greatly, i.e. peroxide value ≤5 mEq/kg in only 7 and ≤10 mEq/kg in 38 fish oils. Compared with equivalent doses of ω-3-acid ethyl esters 90, the mean peroxide intake would be 8.6 ± 6.1 and the alkenal intake 10.9 ± 4.4 times higher in fish oils. Conclusions: Levels of adverse oxidation products should be considered when targeting HUFA deficiency or treating patients with myocardial infarction or high triglycerides.

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Increased enddiastolic wall stress precedes left ventricular hypertrophy in dilative heart failure—Use of the volume-based wall stress index

Cited by 54 publications

References 38 publications

From Heart Failure to Highly Unsaturated Fatty Acid Deficiency and Vice Versa: Bidirectional Heart and Liver Interactions

From Heart Failure to Highly Unsaturated Fatty Acid Deficiency and Vice Versa: Bidirectional Heart and Liver Interactions

Letter by Alter Regarding Article, “Myocardial Fibrosis as a Key Determinant of Left Ventricular Remodeling in Idiopathic Dilated Cardiomyopathy: A Contrast-Enhanced Cardiovascular Magnetic Study”

Replacement of Reduced Highly Unsaturated Fatty Acids (HUFA Deficiency) in Dilative Heart Failure: Dosage of EPA/DHA and Variability of Adverse Peroxides and Aldehydes in Dietary Supplement Fish Oils

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