Contractile reserve

J. A. Fallavollita, B. J. Malm, and J. M. J. Canty, Hibernating myocardiam retains metabolic and contractile reserve despite regional reductions in flow, function, and oxygen consumption at rest, Circ Res 92,48-55 (2003). 

How can the end systolic pressure-volume relations (ESP-ESV) be employed in an assessment of myocardial contractile reserve ... 

This final section explores in a preliminary manner, an approximate method for assessing the contractile state and myocardial contractile reserve in terms of ejection fraction-afterload-preload relationships. The analysis is based on the concept of developed stress defined here to be the difference of end systolic stress and end diastolic stress. 

The SERCA2 homozygous null mouse (—/—) is lethal, but the heterozygous mouse has been useful in assessing the cardiovascular effects of a reduction of SERCA2 protein. Significant alterations in cardiac function were observed (Periasamy et al 1999). However, neither mouse aorta nor portal vein contractility were affected (Weber 1999). We verified that the SERCA protein was indeed reduced so the negative results may indicate that there is a substantial reserve of Ca2+ pump activity. 

Concurrent antiarrhythmic agents Concurrent antiarrhythmic agents may produce enhanced prolongation of conduction or depression of contractility and hypotension, especially in patients with cardiac decompensation. Reserve concurrent use of procainamide with other Class lA antiarrhythmic agents (eg, quinidine, disopyramide) for patients with serious arrhythmias unresponsive to a single drug and use only if close observation is possible. 

Dopamine and dobutamine are sometimes used to stimulate the heart in cases of acute or severe heart failure (see Chapter 20). Dopamine and dobutamine exert a fairly specific positive inotropic effect, presumably through their ability to stimulate beta-1 receptors on the myocardium.60 Other beta-1 agonists (epinephrine, prenalterol, etc.) will also increase myocardial contractility, but most of these other beta-1 agonists will also increase heart rate or have other side effects that prevent their use in congestive heart failure. Dopamine and dobutamine are usually reserved for patients with advanced cases of congestive heart failure who do not respond to other positive inotropic drugs (e.g., digitalis).6,72... 

Sasaki, H., Fukuda, S., Otani, H., Zhu, Li., Yamaura, G., Engelman, R.M., Das, D.K., and Maulik, N. 2002. Hypoxic preconditioning triggers myocardial angiogenesis a novel approach to enhance contractile function reserve in rat with myocardial infarction. J. Mol. Cell. Cardiol. 34 335-348. 

In the hospital, ECG and laboratory tests are performed promptly to determine the subsequent treatment strategy. When car-diomyocytes die, contractile proteins (troponin) or myocardial enzymes (creatine kinase, CK-MB) are liberated and can be detected in blood for diagnostic purposes. Marked elevation of the ST segment in the ECG raises the strong suspicion of a complete occlusion of a coronary artery (ST elevation MI, STEMI). In these MI patients, reperfusion of the affected area as early and as completely as Luellmann, Color Atlas of Pharmacology All rights reserved. Usage subject to terms... 

All were successfully treated with hyperinsulinemia/ euglycemia therapy. The authors described the mechanism of action of this form of therapy, which is mainly related to improvement in cardiac contractility and peripheral vascular resistance and reversal of acidosis. They proposed indications and dosing for this therapy consisting in most cases of intravenous glucose with an intravenous bolus dose of insulin 1 U/kg followed by an infusion of 0.5-1 U/kg/hour until the systolic blood pressure is over 100 mm/Hg and the heart rate over 50/minute. Hyperinsulinemia/euglycemia therapy is currently reserved as an adjunct to conventional therapy and is recommended only after an inadequate response to fluid resuscitation, high-dose calcium salts, and pressor agents. 

This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features - arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve -, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein Ilb/IIIa antagonism. 

Clearly, coronary microembolization is a frequent event in ischemic heart disease, spontaneously in patients with unstable angina / acute coronary syndromes as well as artificially during coronary interventions with typical consequences, such as malignant arrhythmias and contractile dysfunction (Figure 7). The resulting microcirculatory impairment causes patchy microinfarction, and is often associated with coronary hyperemia at baseline and, conversely, transiently reduced coronary reserve. These obser-... 

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