Stress infarcted heart

Dobutamine (dobutrex, others) is indicated for the short-term treatment of cardiac decompensation post cardiac surgery or in patients with congestive heart failure or acute myocardial infarction. An infusion of dobutamine in combination with echocardiography is useful in the noninvasive assessment of patients with coronary artery disease stressing the heart with dobutamine may reveal cardiac abnormalities in selected patients. 

Extension and stress distributions in large acute infarcted hearts... 

Figure 15. Extension and stress distributions in infarcted heart. A. Systolic circumferential extensions in the border zone are larger than normal. B. Circumferential stresses at the edge of the infarct are 3.7 times greater than those at 180°. (Reproduced from Bogen et aL An analysis of the mechanical disdvantage of myocardial infarction in the canine left ventricle, Circ Res 47, 728, 1980 with permission from the American Heart Association.)...

Moderate risk Has three or more risk factors for coronary artery disease Has moderate, stable angina Had a recent myocardial infarction or stroke within the past 6 weeks Has moderate congestive heart failure (NYHA Class 2) Fbtient should undergo a complete cardiovascular work-up and treadmill stress testing to determine tolerance to increased myocardial energy consumption associated with increased sexual activity... 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

T1, as the thallous ion (Tl+), has been used for imaging heart function under stress and rest conditions since about 1975. The thallous ion distributes in viable heart muscle as a potassium ion mimic, through the Na+-K+ ATPase pump. Clinical images with 201T1 show the infarcted regions of the heart as cold spots or without radioactivity. 2 T1 decays by electron capture with a... 

They are used for arrhythmias associated with nervous stress, myocardial infarction, and thyrotoxicosis accompanied by elevated adrenergic activity. Moreover, many antiarrhythmic drugs themselves can cause arrhythmia, especially in patients with ischemic heart disease. The examined 8-adrenergic receptor blockers are an exception. Having said that, practically all )3-adrenergic receptor blockers can be used as antiarrhythmics. 

Enables pretreated cardiac cells to become more resistant to the damage caused by hypoxia-reoxygenation and oxidative stress, enables isolated hearts reperfused in its presence (10 pM) after an ischemic event to display a significant recovery in myocardial performance and to produce a marked and significant reduction in cardiac muscle damage and infarct size [142]... 

The antiplatelet/antithrombotic activity of dipyridamole has been demonstrated in laboratory and in animal models, and has been shown to inhibit platelet aggregation and vessel-wall thrombogenesis [9-11]. Dipyridamole has been given either alone or with aspirin in the management of myocardial infarction and stroke. For the secondary prevention of stroke or transient ischemic attack, the drug may be given as a modified-release preparation in a dose of 200 mg twice daily. Dipyridamole administered intravenously results in a marked coronary vasodilation and is used in stress testing in patients with ischemic heart disease [5]. 

The patient, a 63-year-old Caucasian female, was hospitalized on 4 April 2002 though 10 April 2002 for a non-ST segment elevation myocardial infarction (non-Q-wave MI per chart documentation). She had a negative adenosine stress test after the initial event. Her serum cardiac-specific troponin I (cTnl) concentration 24 hours after her onset of chest pain was 1.4 pg/L (upper limit of normal is 0.3 ng/mL), and her creatine kinase (CK) MB level was 12.5 pg/L (upper limit of normal 6.0 ng/mL). Three days post-event her cTnl level was 0.5 pg/L and her CK-MB level was 4.5 pg/L (Fig. 5-1). MB refers to one of the isoenzyme forms of CK found in serum. The form of the enzyme that occurs in brain (BB) does not usually get past the blood-brain barrier and therefore is not normally present in the serum. The MM and MB forms account for almost all of the CK in serum. Skeletal muscle contains mainly MM, with less than 2% of its CK in the MB form. MM is also the predominant myocardial creatine kinase and MB accounts for 10%-20% of creatine kinase in heart muscle. 

From the influence of the autonomic nervous system it follows that all sympatholytic or sympathomimetic and parasympatholytic or parasympathomimetic drugs can produce corresponding effects on cardiac performance. These possibilities are exploited therapeutically for instance, p-blockers for suppressing excessive sympathetic drive (p. 96) ipratropium for treating sinus bradycardia (p. 108). An unwanted activation of the sympathetic system can result from anxiety, pain, and other emotional stress. In these cases, the heart can be protected from harmful stimulation by psychopharmaceuticals such as benzodiazepines (diazepam and others important in myocardial infarction). 

A phenol peel should of course not be performed after myocardial infarction or cardiac decompensation. Unstable angina also rules out a phenol peel, as the stress associated with a peel could trigger an angina attack. No clear link has ever been established between a personal medical history of a heart condition, if currently stabilized, and the incidence of cardiovascular complications during a phenol peel. Apart from arrhythmias, to the best of my knowledge there is no mention in the literature of any serious heart problems occurring as a complication of a phenol peel. ... 

Joyeux M, Arnaud C, Godin-Ribuot D, Demenge P, Lamontagne D, Ribuot C (2002) Endocannabinoids are implicated in the infarct size-reducing effect conferred by heat stress preconditioning in isolated rat hearts. Cardiovasc Res 55 619-625... 

Mortality secondary to cardiovascular disease is 10 to 30 times greater in dialysis patients than in the general population. In addition to traditional cardiac risk factors such as diabetes, hypertension, hyperlipidemia, tobacco use, and physical inactivity, patients with kidney disease have other unique risk factors. Among these are hyper-homocysteinemia, elevated levels of C-reactive protein, increased oxidant stress, and hemodynamic overload. Complications previously discussed such as anemia and metabolic disorders of CKD are also contributory. In particular, arterial vascular disease (i.e., atherosclerosis) and cardiomyopathy are the primary types of cardiovascular disorders present in the CKD population. These disorders lead to development of ischemic heart disease and its manifestations including myocardial infarction. As a predominant comorbidity, cardiovascular disorders and their sequela are the leading cause of death in the ESKD population. ... 

Two injections (stress and rest) are required in order to differentiate a transient (reversible) from a persistent perfusion defect, which is typical for ischemic heart disease (Borges-Neto et al. 1990 Biill et al. 1996). For verification of a scar after myocardial infarction (nomeversible perfusion defect), one injection at rest (185-300 MBq, resp. 5-8 mCi) may be sufficient. However, it is usually not possible to differentiate an acute myocardial infarction from ischemic defects, which are observed in patients with angina pectoris during chest pain (Tatum et al. 1997). 

Pathological cardiac hypertrophy develops in response to stresses, and can be concentric, eccentric, or both. An excess pressure load placed on the heart, for example, resulting from uncorrected hypertension or valvular disease, results in concentric hypertrophy. This hypertrophy is initially believed to be adaptive, normalizing systolic wall stress, though it is not clear that hypertrophy is necessary to maintain systolic function in the face of moderately elevated pressure loads. Eccentric hypertrophy results most often from volume loads such as those in valvular insufficiency. Einally, the hypertrophy that occurs in the remote noninfarcted myocardium, as part of the remodeling process following a myocardial infarction, may be both concentric and eccentric. 

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