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Session Number : 157000
Session Title: Left-ventricular remodelling
Core syllabus topic : Other
Prof. Otto Martin Hess

Prof. Otto Martin Hess
Date : 3 September 2006

Reported by :
Hess, O.M.
Bern, Switzerland

Left-ventricular remodelling

Left-ventricular (LV) remodelling is defined as a change in LV geometry following acute myocardial infarction or chronic pressure and volume-overload (fig. 1).

The purpose of the present symposium was to discuss the different patterns of LV remodelling (Dr. G. Nicolosi, Italy), to study the effect of microvascular dysfunction and coronary flow (Dr. Colonna, Bari, Italy), and to evaluate the role of cardiac resynchronisation in LV remodelling (Dr. P. Sogard, Denmark). Last but not least the patho-mechanisms of LV remodelling were discussed in diabetic patients with acute myocardial infarction (Dr. S. Solomon, Boston, USA). One important question was addressed during the symposium, what Echo parameter should be used to assess LV-remodelling (LV dimension, LV asynchrony or global LV function). It was suggested that simple Echo parameters should be utilized such as LV ejection fraction, LV dimensions and wall thickness.

According to Dr. Colonna, microvascular dysfunction and coronary flow play a crucial role in the development of LV remodelling. Microvascular dysfunction with low or no coronary flow (no reflow phenomenon) are important determinants for the infarct size and the severity of LV remodelling. Contrast echocardiography was considered by the panel to be best non-invasive technique to assess microvascular dysfunction. The optimal time-point for determination of microvascular dysfunction was, however, unclear but one proposal was to do this when the patient is leaving the hospital.

Asynergy plays an important role in the development of cardiac failure. The occurrence of left bundle branch block is usually associated with a drop in ejection fraction and an increase in LV volume. Resynchronisation with biventricular pacing leads to a reduction in LV volume, an increase in ejection fraction and a decrease in BNP (= brain-natriuretic peptide). Attention should be payed to the exact location and timing of the electrodes (sequential stimulation of the RV and LV electrode) as well as to the AV-delay. The optimal AV-delay can be determined by Doppler-echocardiography. A future approach of biventricular pacing may be the use of multiple endocardial electrodes for optimal re-synchronisation of the left ventricle.

Diabetes plays an important role in the development of heart failure and LV remodelling. An increase in mortality has been demonstrated in diabetic patients after acute myocardial infarction, typically in those who develop congestive heart failure. An interesting observation was reported at the symposium that diabetic patients show less remodelling after myocardial infarction than non-diabetic patients. The exact mechanism of this observation is not clear but may be due to structural changes of the myocardium with an elevation of diastolic filling pressures.

Conclusion

The different patterns of LV remodelling after acute myocardial infarction have been discussed during the symposium and the role of microvascular dysfunction and conorary flow has been addressed. An intriguing observation was made that diabetic patients show less LV remodelling after myocardial infarction than non-diabetics. The nature of this finding is not clear but may be to structural changes associated with diabetes mellitus.

Furthermore, the beneficial effect of cardiac resynchronisation was discussed during the meeting and the role of sequential stimulation of the RV and LV electrode was addressed. The best approach to resynchronize the left ventricle is the use of multiple endocardial electrodes.



 
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