What is left ventricle end diastolic pressure (LVEDP)?

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Left Ventricular End-Diastolic Pressure (LVEDP)

Left ventricular end-diastolic pressure (LVEDP) is the pressure within the left ventricle at the end of diastole, just before contraction begins, and represents an important hemodynamic marker of left ventricular performance that affects coronary perfusion and is a key indicator of diastolic function. 1, 2

Definition and Physiological Significance

  • LVEDP is one of several measurements that fall under the broader term "LV filling pressures," which can also refer to mean pulmonary capillary wedge pressure (PCWP), mean left atrial pressure (LAP), LV pre-A pressure, and mean LV diastolic pressure 1
  • LVEDP specifically measures the pressure in the left ventricle at the end of ventricular filling, just before systole begins 3
  • In normal cardiac function, LVEDP typically ranges from 8-12 mmHg, with values above 15 mmHg generally considered elevated 4
  • LVEDP directly affects coronary perfusion pressure and is a critical determinant of myocardial oxygen supply 2

Clinical Significance

  • Elevated LVEDP is a hallmark of diastolic dysfunction and can be an early indicator of heart failure, particularly heart failure with preserved ejection fraction (HFpEF) 1, 3
  • In the early stages of diastolic dysfunction, LVEDP may be the only abnormally elevated pressure due to a large atrial pressure wave, while mean PCWP and LAP remain normal 1
  • Elevated LVEDP (≥26 mmHg) in patients undergoing elective percutaneous coronary intervention is associated with higher rates of in-hospital adverse outcomes, including death 2
  • Following myocardial infarction, elevated LVEDP is common but not an independent predictor of subsequent heart failure risk when adjusted for other known predictors of cardiac risk 4

Measurement Methods

  • The gold standard for measuring LVEDP is through cardiac catheterization, where a catheter is placed directly into the left ventricle 5
  • Non-invasive estimation of LVEDP can be performed using echocardiography, particularly with Doppler techniques 6
  • Doppler signals that correlate best with LVEDP include mitral peak A velocity at tips level, A-wave duration at the annulus, pulmonary vein peak Ar velocity, and tissue Doppler-derived mitral annular a' velocity 1
  • The ratio of passive and active components of mitral flow shows a significant linear correlation with LVEDP, with mitral flow ratios greater than 2 typically associated with LVEDP greater than 20 mmHg 6

Clinical Applications

  • Assessment of LVEDP is integral to the evaluation of patients presenting with symptoms of dyspnea or heart failure 1
  • Elevated LVEDP in the absence of increased LV end-diastolic volume provides strong evidence for well-developed diastolic dysfunction 1
  • In patients with ST-segment elevation myocardial infarction (STEMI), elevated LVEDP (≥20 mmHg) is an independent predictor of mortality and heart failure 5
  • Therapeutic interventions aimed at reducing elevated LVEDP, such as administration of glyceryl trinitrate plus furosemide, have been shown to safely reduce LVEDP in post-primary PCI STEMI patients 5

Clinical Pitfalls and Considerations

  • Radiographic assessment of pulmonary hemodynamics has limited correlation with LVEDP, with 38% of patients with LVEDP over 20 mmHg not showing signs of congestive heart failure on chest radiographs 7
  • LVEDP measurements can be affected by mechanical ventilation, heart rate, rhythm abnormalities, and age-related changes in diastolic function 3
  • The relationship between LVEDP and left ventricular ejection fraction is not always straightforward, as demonstrated by the lack of correlation in some studies 5
  • When interpreting LVEDP, it should always be considered in the context of other clinical parameters and echocardiographic measurements 1

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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