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- Diastolic dysfunction refers to impaired ventricular relaxation and filling resulting in a higher end-diastolic pressure for a given end-diastolic volume, which leads to pulmonary venous congestion.
- Distinguishing diastolic heart failure (DHF) from systolic heart failure (SHF) is important because of differences in treatment and prognosis.
- Impaired relaxation – common in ischemia (reduced ATP), worse if hypertrophy
- Impaired peak LV filling rate – inadequate transmitral pressure gradient due to raised LVP or inability to generate negative LVP (suction) – the latter is achieved by titin (a protein) which is compressed in systole and forcefully re-expands in early diastole like a spring
- Stiffness of LV – fibrosis and hypertrophy
- Constriction – pericardial or compression from dilated RV
- ischemic heart disease
- Restrictive cardiomyopathy
- Hypertrophy including HCM
- Aortic stenosis
- Occurs between closure of the aortic valve to closure of the MV
- Relaxation begins when maximal shortening and LV pressure has been reached, shortly before ejection has finished, but clinically it begins with AV closure
- Early diastolic relaxation (lusitropy) is energy dependent (requires ATP for sequestration of calcium and actin-myosin dissociation)
- Compliance is the volume/pressure relationship and is an intrinsic property of the heart
4 phases of flow with 2 main components: active relaxation (early diastole) and passive compliance (mid and late diastole)
- Isovolumetric relaxation – no flow
- Early rapid filling down transmitral pressure gradient
- Diastasis – low flow in mid diastole
- Late rapid filling – atrial contraction – contributes about 30% of LV filling
- The normal LV can accommodate a wide range of venous return without elevation of filling pressures.
- Dysfunction results from both impaired active relaxation and reduced passive compliance.
- Just like there are RWMAs in systolic failure, diastolic failure also demonstrates regional variations.
- The overall effect is impaired LV filling and a higher LVEDP for a given LVEDV which leads to pulmonary venous congestion.
- Atrial fibrillation – Atrial contribution to filling more important as LVP rises but Afib very common as atrial dilatation results from elevated LVP
- Tachycardia – reduces time for the compromised diastolic filling
- Hypertension – increased LV wall tension (afterload) impairs relaxation
- often asymptomatic
- Symptoms are the same as for LV systolic failure
- 40% of those with symptoms of HF have preserved EF
- All patients with systolic dysfunction due to heart disease will have diastolic dysfunction
DD made worse by:
- LV catheterisation is gold standard but ECHO is more practical.
- Treat underlying cause – hypertension control, IHD, AF
- ACEIs, AT2R antagonistss and calcium channel blockers can all reduce hypertension and reverse LVH
- Restore sinus rhythm if possible
- Af usually requires rate control as dilated LA prevents maintenance of sinus rhythm. Avoid digoxin as increased inotropy is not required and calcium uptake is impaired.
- Treatment of IHD will provide increase O2 supply, improving active relaxation and reducing LVEDP and remodelling.
- Activation of RAS (in an effort to increase LAP) cause progression of cardiomyopathy and remodelling. Treatments to prevent this (eg ACEi should be used cautiously as the LV is very preload dependent).
- Exercise will reduce resting HR and improve Ca uptake.
References and Links
- Kapila R, Mahajna RV. Diastolic dysfunction. Contin Educ Anaesth Crit Care Pain (2009) 9 (1): 29-33. doi: 10.1093/bjaceaccp/mkn046 [Free Fulltext]