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Ventriculo-arterial coupling in valvular heart disease

Ventriculo-arterial coupling in valvular heart disease. Renato Razzolini. PRESSURE-VOLUME LOOP. PERIPHERAL (ARTERIOLAR) RESISTANCE (R). Peripheral (arteriolar) Resistance is the ratio between mean aortic pressure (Pao) and mean left ventricular antegrade output (Qa). EFFECTIVE AFTERLOAD (Ea).

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Ventriculo-arterial coupling in valvular heart disease

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  1. Ventriculo-arterial coupling in valvular heart disease Renato Razzolini

  2. PRESSURE-VOLUME LOOP

  3. PERIPHERAL (ARTERIOLAR) RESISTANCE (R) • Peripheral (arteriolar) Resistance is the ratio between mean aortic pressure (Pao) and mean left ventricular antegrade output (Qa).

  4. EFFECTIVE AFTERLOAD (Ea) • Effective afterload is the ratio between left ventricular end systolic pressure (Pes) and left ventricular stroke volume (SV).

  5. CONTRACTILITY (Es) • Contractility is the ratio between left ventricular end systolic pressure (Pes) and left ventricular end systolic volume (ESV). Pes Ea = ESV

  6. Pao: Mean aortic pressure Plv: Mean left ventricular pressure Pes: Left ventricular end systolic pressure Plvs: Mean left ventricular systolic pressure

  7. QUESTION # 1 • Is there any relationship between Resistance (R), and Effective Afterload (Ea)? • Q = SV * HR • Pes/R = SV * HR • Pes/SV = R * HR; Ea = R * HR • HR = Heart Rate; Q = Cardiac output; SV = Stroke volume

  8. Ea induced modifications on pressure-volume loop Ees = Pressione sistolica / volume telesistolico Ea = Pressione sistolica / gettata sistolica Normalmente: Ea/Ees =<1 Nello scompenso: Ea/Ees > 1 PRESSURE Ees Ea VOLUME LVEDV Ea = R * HR

  9. ANSWER #1 • The relation between Peripheral Resistance (R) and Ea is linear only in normal subjects, not in patients with diastolic overload.

  10. EFFECTIVE AFTERLOAD/RESISTANCE

  11. QUESTION #2 • What is the nature of the relation between Resistance (R) and Effective Afterload (Ea), both in normal and in diastolic overloaded hearts?

  12. We can answer this question by having recourse to the Windkessel model, which relates left ventricular end systolic pressure (Pes, Plvs, dicrotic notch) to the arterial Resistance (R) and Compliance (C), and to the duration of systole and diastole.

  13. QUESTION #3 • What can be a practical application of these concepts?

  14. EXAMPLES OF CLINICAL APPLICATIONS • 1. Measurement of the left ventricular end systolic pressure • 2. Measurement of peripheral Resistance in aortic insufficiency • 3. Estimation of regurgitating volumes in mitral and aortic insufficiency • 4. Prediction of the effects of interventions on left ventricular function

  15. In acute setting, a decrease in Ea results in an increase in left ventricular end diastolic volume, unless either left ventricular end systolic pressure decreases, or the heart rate increases (the increase in heart rate makes Ea to increase) • LVEDV = Pes * (1/Ea + 1/Es)

  16. Ea induced modifications on pressure-volume loop Ees = Pressione sistolica / volume telesistolico Ea = Pressione sistolica / gettata sistolica Normalmente: Ea/Ees =<1 Nello scompenso: Ea/Ees > 1 PRESSURE Ees Ea VOLUME LVEDV Ea = R * HR

  17. Modifications of Ea on pressure-volume loop Ea = R*HR Ea Ea' Es Control Ea" Vasodilation ... & decreased Pes PRESSURE ...& increased HR LVEDV ' VOLUME LVEDV" LVEDV

  18. HYDRALAZINE IN MITRAL INSUFFICIENCY Greenberg BH et al: Beneficial effects of Hydralazine in severe mitral regurgitation. Circulation 1978; 58:273-279.

  19. HYDRALAZINE IN AORTIC INSUFFICIENCY Greenberg BH et al: Mechanisms for improved cardiac performance with arteriolar dilators in aortic insufficiency. Circulation 1981; 63:263-268.

  20. NIFEDIPINE IN AORTIC INSUFFICIENCY Scognamiglio R et al: Long-term nifedipine unloading therapy in asymptomatic patients with chronic severe aortic regurgitation. J Am Coll Cardiol 1990; 16:430-432.

  21. conclusions Long-term vasodilator therapy with nifedipine or enalapril did not reduce or delay the need for aortic-valve replacement in patients with asymptomatic severe aortic regurgitation and normal left ventricular systolic function. Furthermore, such therapy did not reduce the aortic regurgitant volume, decrease the size of the left ventricle, or improve left ventricular function. n engl j med 353;13-29, 2005

  22. MITRAL INSUFFICIENCY

  23. MITRAL INSUFFICIENCY

  24. AORTIC INSUFFICIENCY

  25. AORTIC INSUFFICIENCY

  26. SOURCE RESISTANCE/EFFECTIVE AFTERLOAD

  27. CONCLUSIONS • Effective Afterload - Contractility paradigm describes ventriculo-arterial coupling in valvular heart diseases. • It can predict cardiovascular behavior after interventions that alter contractility, peripheral resistances or heart rate.

  28. SOURCE RESISTANCE • NORMAL SUBJECTS (N) 0.765 • MITRAL INSUFFICIENCY (M) 0.453 • AORTIC INSUFFICIENCY (A) 0.612 Test ANOVA: N <> M & A; p = 0.025

  29. CONCLUSIONS • It demonstrates that mean left ventricular systolic pressure equals left ventricular end systolic pressure in normal and diseased patients. • It allows a correct determination of peripheral resistance in aortic insufficiency.

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