Measurement of Myocardial Contractility in the Ischemic Heart -A Disease Immanent Uncertainty (Diagnostics of Ischemic Heart Disease) Part 3

Dobutamine induces ineffective work in regional ischaemic myocardium: An experimental strain rate imaging study

This study is to answer the question as to whether the results of the previous study can also be reflected by parameters of regional contractility.

In an animal experiment, 11 Gottinger minipigs were studied in a closed chest preparation. We advanced a coronary occlusion-perfusion catheter into the ramus circumflexus of the left coronary artery from the arteria femoralis. This catheter makes it possible to occlude a coronary artery while at the same time perfusing it with arterial blood using an adjustable roller pump. Standardized reduction of myocardial wall motion in the circulation area of the coronary artery was monitored by determining the strain rate. Apart from that, radial strain of the myocardium during systole was also determined. Strain is a unit of measurement for myocardial deformation. As the arteria femoralis was occupied by the catheter, we advanced the conductance catheter through the right arteria carotis communis.

The results show that a decrease of radial strain in the ischemic region can be documented under regional ischemia. Parallel to this, regional ischemia led to an increase in radial strain in the non ischemic myocardium. The stimulation of contractility with dobutamine intensifies the effect.

The present results confirm those of the previous study, i.e. that regional ischemia of the myocardium of 30% does not lead to a decrease of global contractility because contractility of the myocardium of the non-ischemic region is increased in a compensatory way. The increase of internal flow fraction is based on this effect, as has been shown in the previous study.


The relationship between carotid arterial flow and the left ventricular area is valid to indicate contractility in states of cerebral autoregulation and decreased arterial pressure

The present study is based on the question as to whether both measuring methods correspond under the condition of an arterial hypotension. Hypotension can activate mechanisms which, independent of systemic blood pressure, ensure constant blood flow in important organs such as the heart. To determine the flow-area relationship, we measure flow velocity in large vessels which supply the brain with blood; for this reason these mechanisms could have an effect on the flow-area relationship.

In an animal experiment, we studied 9 merino sheep and measured cortical microperfusion (flux) with the laser Doppler and we also determined tissue oxygen partial pressure (p(ti)O2) and tissue metabolism through microdialysis. We proceeded as in a validation study, the difference being that we fixed the TEE probe onto the myocardium with a minithoracotomy.

Arterial blood pressure was, on the one hand, decreased by esmolol and on the other hand by the pure vasodilator sodium nitroprusside. Both pharmaceuticals were dosed in such a way that a mean arterial pressure of 50mmHg could be maintained for 20 minutes.

The table shows that the hypotension triggered by sodium nitroprusside did not lead to any other changes of the circulatory system and of the cortical and myocardial parameters. The hypotension triggered by esmolol, however, led to a decrease in cardiac output and to an increase in LV end-diastolic pressure. This was associated with a decrease in cortical microcirculation as well as with a decrease in tissue oxygen partial pressure. During the decrease in tissue oxygen partial pressure, the metabolites of the anaerobic metabolism increased. Furthermore an increase in internal flow fraction (IFFsys) could be observed, indicating myocardial wall motion abnormalities. The hypotension triggered by esmolol led to a critical decrease of oxygen being supplied to the cortex and to the myocardium.

As in the previous studies, a linear correlation between flow-area relationship and LV pressure could be detected under the influence of sodium nitroprusside. The correlation between the two relationships was acceptable as the Bland-Altman analysis shows. The decrease of contractility induced by esmolol was also detected through the flow-area relationship. But the degree of correlation and the degree of correspondence of both parameters decreased significantly. This decrease probably results from an increase of the internal flow fraction as an indication of myocardial wall motion abnormalities. This correlation could already be detected in the previous studies. It remains unclear, however, which hemodynamic constellation led to the wall motion abnormalities – the increase in end-diastolic volume and/ or the decrease of cardiac output. Both parameters determine myocardial perfusion.

Diagram for the experiment set-up of the study "The Relationship between Carotid Arterial Flow and the Left Ventricular Area is valid to indicate contractility in states of cerebral autoregulation and decreased arterial pressure

Fig. 6. Diagram for the experiment set-up of the study "The Relationship between Carotid Arterial Flow and the Left Ventricular Area is valid to indicate contractility in states of cerebral autoregulation and decreased arterial pressure

An increase in end-diastolic volume is connected with an increase in left ventricular radius. According to the law of Laplace, the increase in radius is tantamount to an increase in myocardial wall tension in diastole. During diastole the myocardium is perfused an increase in wall tension can lead to a decrease of coronary blood flow which means that oxygen supply is higher than oxygen demand. In this context, myocardial wall motion abnormalities can occur as an indication of hypoperfusion. A decrease in cardiac output is directly connected to a decrease of oxygen supply to all organs, i.e. also to the myocardium, which can result in insufficient oxygen supply.

The results of the study carried out showed that a valid assessment of myocardial contractility is possible with the flow-area relationship.

Validational study during arterial hypotension - Results

Fig. 6b. Validational study during arterial hypotension – Results

Association of increased myocardial contractility and elevated end-diastolic wall tension with short-term myocardial ischemia: A pressure-volume analysis

The present study is to answer the question whether myocardial hypoperfusion can be triggered by an LV hypervolemia, even if arterial pressure as well as cardiac output are in an "adequate" range – as literature usually calls it.

To answer this question, 15 Gottinger minipigs were studied in an open chest preparation. A catheter was placed in the arteria femoralis to measure pressure and a probe ,similar to those used for transoesophageal echocardiography, was fixed on the myocardium. A microtip catheter was inserted from the apex of the left ventricle for continuous pressure measurement. A catheter for microdialysis was implanted into the myocardium in the flow area of the left coronary artery. Finally, the arteria carotis communis was dissected to fix a U-shaped 8-MHz CW Doppler probe on it. A catheter in the femoral vein was used for pharmacological interventions.

Myocardial contractility was increased permanently through continuous application of dobutamine. A steady state was assumed after 20 minutes. Esmolol was administered in such a way that the heart rate – in relation to frequency – was lowered by at least 25% for 20 minutes under continuous infusion of dobutamin. Subsequently esmolol application was stopped so that dobutamin could again unfold its contractility-increasing effect. For comparison, only Esmolol was subsequently administered to another group – to the same amount as dobutamine and esmolol had been administered in the dobutamin-esmolol group. As expected, the table shows that when dobutamine and esmolol are administered at the same time, the heart rate decreases and contractility decreases later as well. Through the decrease in heart rate, LV volume increases in this phase and thus – according to the law of Laplace – diastolic myocardial wall tension increases as well. Dobutamine initially stimulates contractility but despite sufficient arterial pressure and cardiac output, oxygen supply is still lower than oxygen demand. Oxygen demand is then lowered by the decrease in contractility and the indications of hypoperfusion recede under identical wall tension. When the effect of esmolol starts to wear off, the contractility-stimulating effect of dobutamin comes back first and later the heart rate increases again. During this phase, increased wall tension leads to myocardial hypoperfusion again. Esmolol alone induces increased wall tension but no myocardial hypoperfusion.

The results of the present study show that an increase in myocardial wall tension alone is not necessarily associated with myocardial hypoperfusion. If, however, oxygen demand increases in this situation, or, as in the previous study, cardiac output and arterial pressure are reduced, the oxygen supply to the myocardium can sink below its oxygen demand. In this context, myocardial wall motion disorders can form as an indication of such an imbalance which in turn can lower the correlation of the two relations.

Conclusion and outlook

The results of the examination carried out allow the conclusion that a valid estimation of myocardial contractility is possible. Myocardial wall motion abnormalities limit the measuring accuracy of this new procedure. These myocardial wall motion abnormalities can occur if increased LV end-diastolic volume is associated with low cardiac output or an increased myocardial oxygen requirement.

In further investigations we would like to try to answer the question as to whether the acute afterload reduction necessary for the determination of elastance can also be induced through a Valsalva maneuver.

By using a 3-dimensional transoesophageal echocardiography, we would like to answer the question if measuring accuracy can possibly be significantly improved. On the one hand, using 3-dimensional echocardiography, similar to what is possible with a conductance catheter, could make it possible to determine internal flow fraction and consequently to develop a corrective factor for measurement. On the other hand, using 3-dimensional echocardiography makes it possible to estimate intraventricular volumes much more precisely than with the cross-sectional LV area.

Finally the use of this procedure should be verified in clinical studies.

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