Ischemic myocardial dysfunction

Skeletal myoblast intramyocardial injection for ischemic myocardial dysfunction... 

C. I. Pantos, C. H. Davos, H. C. Carageorgiou, D. V. Varonos, D. V. Cokkinos, Ischemic preconditioning protects against myocardial dysfunction caused by ishaemia in isolated hypertrophied rat hearts, Basic Res Cardiol 91, 444-449 (1996). 

Piezoelectric sensors are useful for assessment of myocardial function after acute ischemic injury (as a function of occluding regional coronary blood flow). Figure 2.21 shows preischemic base line conditions and postischemic myocardial dysfunction. Ventricular pressure-segmental length loops and end-systolic pressure-length relationships under control conditions (preischemia) and 15 min after coronary occlusion (ischemia) are illustrated. 

Figure 2.19 An experimental preparation with left anterior descending coronary pneumatic occluder, subendocardial piezoelectric dimensional sensors in ischemic and non-ischemic zones and left ventricular and pleural pressure sensors. (From D D Glower, J A Spratt, J S Kabas, J W Davis and J S Rankin Quantification of regional myocardial dysfunction after acute ischemic injury, 1988 Am. J. Physiol. 255 Heart Circ. Physiol. 24) H85-H93 1988.)... 

Introduction A number of risk factors have been identified for perioperative cardiovascular complications, and are used for risk stratification of patients for surgery. These include a history of ischemic heart disease, myocardial dysfunction, or a history of compensated heart failure, a history of cerebrovascular disease, diabetes mellitus, and renal insufficiency. Patients in these risk categories are very likely to be taking one or more antihypertensive medications, both to control arterial hypertension and as therapy for other underlying diseases. Preoperative evaluation is an opportunity to optimize control of cardiovascular risk factors and review medication requirements. 

To control risk factors and prevent major adverse cardiac events, statin therapy should be considered in all patients with ischemic heart disease, particularly in those with elevated low-density lipoprotein cholesterol. In the absence of contraindications, angiotensin-converting enzyme inhibitors should be considered in ischemic heart disease patients who also have diabetes melli-tus, left ventricular dysfunction, history of myocardial infarction, or any combination of these. Angiotensin receptor blockers... 

Ventricular premature depolarizations occur with variable frequency, depending on underlying comorbid conditions. The prevalence of complex or frequent VPDs is approximately 33% and 12% in men with and without CAD, respectively 34 in women, the prevalence of complex or frequent VPDs is 26% and 12% in those with and without CAD, respectively.35 Ventricular premature depolarizations occur more commonly in patients with ischemic heart disease, a history of myocardial infarction, and HF due to LV dysfunction. They may also occur as a result of hypoxia, anemia, and following cardiac surgery. 

VF is electrical anarchy of the ventricle resulting in no cardiac output and cardiovascular collapse. Sudden cardiac death occurs most commonly in patients with ischemic heart disease and primary myocardial disease associated with LV dysfunction. VF associated with acute MI may be classified as either (1) primary (an uncomplicated MI not associated with heart failure [HF]) or (2) secondary or complicated (an MI complicated by HF). 

Goal BP values are <140/90 for most patients, but <130/80 for patients with diabetes mellitus, significant chronic kidney disease, known coronary artery disease (myocardial infarction [MI], angina), noncoronary atherosclerotic vascular disease (ischemic stroke, transient ischemic attack, peripheral arterial disease [PAD], abdominal aortic aneurysm), or a 10% or greater Framingham 10-year risk of fatal coronary heart disease or nonfatal MI. Patients with LV dysfunction have a BP goal of <120/80 mm Hg. 

Myocardial ischemia and infarction cause abnorma myocardial metabolism, decreased left ventricular (LV) systolic function, diastolic dysfunction, congestive heart failure, and decreased survival. Consequently, revascularization techniques, either surgical or catheter based, have become integral to treatment of severe ischemic heart disease. 

Size and severity of ischemic areas correlate well with mortality in both stable CAD populations [70] and after myocardial infarction [71]. Moreover, the presence of ischemia in a dysfunctional segment of myocardium is a powerful predictor of functional recovery. Up to 83% of regions with reversible defects (ischemia) will improve with revascularization compared to only 33% for regions where no reversibility was demonstrated [72]. In patients with heart failure, viable poorly contracting myocardium correlates with recovery... 

Gerber BL, Vanoverschelde JL, Bol A, Michel C, Labar D, Wijns W et al. Myocardial blood flow, glucose uptake, and recruitment of inotropic reserve in chronic left ventricular ischemic dysfunction. Imphcations for the pathophysiology of chronic myocardial hibernation. Circulation 1996 94 651-659... 

A review of trials has suggested that vasopressin is more likely to cause adverse effects at doses of 0.04 U/minute or more when it is used to treat septic shock mesenteric ischemia and cardiac dysfunction and ischemia were particularly associated with high doses (30). The authors suggested that limiting the dosage to 0.03 U/minute may minimize these effects. This suggestion has been supported by a retrospective audit of the effects of continuous vasopressin infusion in septic shock in 102 men and women, mean age 53 years (31). There were adverse events that may have been linked to vasopressin in 18 patients cardiac arrest (n = 9) ischemic/mottled digits (n = 8) myocardial infarction (n = 1) and hyponatremia (n = 1). Adverse events occurred with doses of vasopressin of 0.04 units/minute and over, except in one patient (dose not stated). 

Decreased cardiac performance. Any number of factors that affect cardiac pumping ability may be responsible for initiating a change in myocardial performance. Factors such as ischemic heart disease, myocardial infarction, valve dysfunction, and hypertension may all compromise the heart s pumping ability.29 53 71 Also, cardiomyopathy may result from other diseases and infections.13... 

The mechanism responsible for PBN-induced cardiac dysfunction is unclear. In previous studies on free radical generation in the ischemic canine heart, hearts were perfused with 50 mmol/1 PBN and 50 mmol/1 MNP for 30 minutes prior to ischemia. It is possible that these high concentrations caused significant cardiac dysfunction and even injury to the heart prior to the ischemic insult. Similar concerns have also been expressed by Bolli et al. [110], In these studies the spin adduct subsequently detected in myocardial tissue by ESR spectroscopy during ischemia may have arisen, in part, as a consequence of the toxic effects of the spin traps. 

Limburg M, Wijdicks EF, Li H (1998). Ischemic stroke after surgical procedures clinical features, neuroimaging and risk factors. Neurology 50 895-901 Loh E, St John Sutton MS, Wun CC et al. (1997). Ventricular dysfunction and the risk of stroke after myocardial infarction. New England Journal of Medicine 336 251-257... 

In isolated perfused hearts, ventricular dysfunction may be due to myocardial stunning or lethal cell injury. In the Langendorff perfused ischemic rat hearts, ATP concentrations decrease rapidly to 60% in the first minute, with a rapid secondary decrease by 13 min due to contracture (33). Recovery from stunned to normal myocardium requires 24-48 h in the in vivo reperfused heart with coronary artery occlusion of 2-20 min (34). Dobrinina et al. (11) showed that neutral liposomes preserved liver integrity in rats subjected to hepatotropic poisons by non-specific mechanisms. However, histochemical infarct size data do not support this hypothesis in the myocardium (Fig. 3b). 

Stunning is related to decreased availability of adenosine triphosphate (ATP) to the myofibrils injury of the contractile apparatus alterations in calcium homeostasis with calcium overload and burst of free radicals. The earliest consequence of severe ischemia is contractile dysfunction, occurring within 6-10 s of ischemia. Loss of tetrazolium staining after ischemic injury occurs due to loss of cofactor NADH and reflects lack of dehydrogenase enzymatic activity. The total NAD and NADH contents are relatively stable in the early phases of ischemia but decrease after irreversible myocardial injury. 

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