A new methodological approach to assess cardiac work by pressure–volume and stress–length relations in patients with aortic valve stenosis and dilated cardiomyopathy
- 229 Downloads
In experimental animals, cardiac work is derived from pressure–volume area and analyzed further using stress–length relations. Lack of methods for determining accurately myocardial mass has until now prevented the use of stress–length relations in patients. We hypothesized, therefore, that not only pressure–volume loops but also stress–length diagrams can be derived from cardiac volume and cardiac mass as assessed by cardiac magnetic resonance imaging (CMR) and invasively measured pressure. Left ventricular (LV) volume and myocardial mass were assessed in seven patients with aortic valve stenosis (AS), eight with dilated cardiomyopathy (DCM), and eight controls using electrocardiogram (ECG)-gated CMR. LV pressure was measured invasively. Pressure–volume curves were calculated based on ECG triggering. Stroke work was assessed as area within the pressure–volume loop. LV wall stress was calculated using a thick-wall sphere model. Similarly, stress–length loops were calculated to quantify stress–length-based work. Taking the LV geometry into account, the normalization with regard to ventricular circumference resulted in “myocardial work.” Patients with AS (valve area 0.73 ± 0.18 cm2) exhibited an increased LV myocardial mass when compared with controls (P < 0.05). LV wall stress was increased in DCM but not in AS. Stroke work of AS was unchanged when compared with controls (0.539 ± 0.272 vs 0.621 ± 0.138 Nm, not significant), whereas DCM exhibited a significant depression (0.367 ± 0.157 Nm, P < 0.05). Myocardial work was significantly reduced in both AS and DCM when compared with controls (129.8 ± 69.6, 200.6 ± 80.1, 332.2 ± 89.6 Nm/m2, P < 0.05), also after normalization (7.40 ± 5.07, 6.27 ± 3.20, 14.6 ± 4.07 Nm/m2, P < 0.001). It is feasible to obtain LV pressure–volume and stress–length diagrams in patients based on the present novel methodological approach of using CMR and invasive pressure measurement. Myocardial work was reduced in patients with DCM and noteworthy also in AS, while stroke work was reduced in DCM only. Most likely, deterioration of myocardial work is crucial for the prognosis. It is suggested to include these basic physiological procedures in the clinical assessment of the pump function of the heart.
KeywordsCardiac work Stroke work Myocardial work Pressure–volume diagram Stress–length diagram Cardiac MRI Wall stress
The study was supported by a Research Grant of the University Medical Center Giessen and Marburg.
- 2.Alter P, Rupp H, Czerny F, Vollrath A, Rominger MB, Maisch B (2006) Relation of ventricular wall stress and autonomic tone in patients with dilated cardiomyopathy assessed by cardiac magnetic resonance imaging. Eur Heart J 27Supp:P4039Google Scholar
- 7.Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, Domanski M, Troutman C, Anderson J, Johnson G, McNulty SE, Clapp-Channing N, Davidson-Ray LD, Fraulo ES, Fishbein DP, Luceri RM, Ip JH (2005) Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 352(3):225–237PubMedCrossRefGoogle Scholar
- 12.Carroll JD, Hess OM (2004) Assessment of normal and abnormal cardiac function. In: Zipes DP, Libby P, Bonow RO, Braunwald E (eds) Braunwald’s heart disease. A textbook of cardiovascular medicine. Elsevier, Pennsylvania, pp 491–507Google Scholar
- 15.Frank O (1895) Zur Dynamik des Herzmuskels. Z Biol 32:370–382Google Scholar
- 29.Roten L, Nemoto S, Simsic J, Coker ML, Rao V, Baicu S, Defreyte G, Soloway PJ, Zile MR, Spinale FG (2000) Effects of gene deletion of the tissue inhibitor of the matrix metalloproteinase-type 1 (TIMP-1) on left ventricular geometry and function in mice. J Mol Cell Cardiol 32(1):109–120PubMedCrossRefGoogle Scholar
- 38.Strauer BE, Beer K, Heitlinger K, Hofling B (1977) Left ventricular systolic wall stress as a primary determinant of myocardial oxygen consumption: comparative studies in patients with normal left ventricular function, with pressure and volume overload and with coronary heart disease. Basic Res Cardiol 72(2–3):306–313PubMedCrossRefGoogle Scholar