Cardiac ischaemia

Dopamine is an intermediate product in the biosynthesis of noradrenaline. Furthermore it is an active transmitter by itself in basal ganglia (caudate nucleus), the nucleus accumbens, the olfactory tubercle, the central nucleus of the amygdala, the median eminence and some areas in the frontal cortex. It is functionally important, for example in the extra-pyramidal system and the central regulation of emesis. In the periphery specific dopamine receptors (Di-receptors) can be found in the upper gastrointestinal tract, in which a reduction of motility is mediated, and on vascular smooth muscle cells of splanchnic and renal arteries. Beside its effect on specific D-receptors, dopamine activates, at higher concentrations, a- and -adrenoceptors as well. Since its clinical profile is different from adrenaline and noradrenaline there are particular indications for dopamine, like situations of circulatory shock with a reduced kidney perfusion. Dopamine can dose-dependently induce nausea, vomiting, tachyarrhythmia and peripheral vasoconstriction. Dopamine can worsen cardiac ischaemia. 

Cardiac ischaemia may trigger abnormal electrical activity, causing fibrillation. Defibrillators deliver a large DC shock across the heart (cardioversion), to arrest abnormal activity and allow re-establishment of sinus rhythm. 

Angiogenesis for cardiovascular disease. Angiogenesis represents an excellent therapeutic target for the treatment of cardiovascular disease, namely the production of new collateral vessels to overcome the ischaemic insult. However, despite the large number of pre-clinical trials in animal models of cardiac ischaemia, no therapy designed to stimulate angiogenesis in underperfused tissue has yet become viable in man. 

ANTIANGINAL AGENTS are used to relieve angina pectoris, an intense pain due to cardiac ischaemia, which is especially pronounced in exercise angina. The disease state often results from atheroma a degeneration of the lining of the arteries of the heart due to build-up of fatty deposits. 

Rudolph, V., T. K. Rudolph, F. J. Schopfer et al. 2010. Endogenous generation and protective effects of nitro-fatty acids in a murine model of focal cardiac ischaemia and reperfusion. Cardiovasc Res 85 (l) 155-66. 

While the authors would recommend routine use of hyoscine butylbromide prior to CT colonography, some caution needs to be exercised prior to administration. Glaucoma, cardiac ischaemia and urinary retention may all be precipitated and minor self limiting effects of dry mouth and blurred vision are also associated. Consequently, patients should be questioned about any relevant past medical history and advised not to drive for a short time following administration. 

O Shea L, Oloko S, Miranda J. Adrenaline-induced cardiac ischaemia treating anaphylaxis in two elderly patients. Int J CUn Pract 2009 63(9) 1394. 

These symptoms should be described as a possible reaction to amiodarone infusion. However, it is of crucial importance to be aware of this phenomenon as acute epigastric pain is implicated in the differential diagnosis of cardiac ischaemia [19]. 

These detailed cell models can be used to study the development in time of processes like myocardial ischaemia (a reduction in coronary blood flow that causes under-supply of oxygen to the cardiac muscle), or effects of genetic mutations on cellular electrophysiology. They allow to predict the outcome of changes in the cell s environment, and may even be used to assess drug actions. 

While the ECG is an invaluable tool for the observation of heart rate and rhythm, as well as for the diagnosis of conduction abnormalities, ischaemia, and infarcts, its detailed interpretation is not without pitfalls. One reason for this is that different changes in cardiac cellular behaviour may give rise to very similar effects on the ECG. This makes it difficult to draw conclusions from a patient s ECG to the underlying (sub-)cellular mechanisms. This issue is usually referred to as the inverse problem. ... 

NADH, which enters the Krebs cycle. However, during cerebral ischaemia, metabolism becomes anaerobic, which results in a precipitous decrease in tissue pH to below 6.2 (Smith etal., 1986 Vonhanweh etal., 1986). Tissue acidosis can now promote iron-catalysed free-radical reactions via the decompartmentalization of protein-bound iron (Rehncrona etal., 1989). Superoxide anion radical also has the ability to increase the low molecular weight iron pool by releasing iron from ferritin reductively (Thomas etal., 1985). Low molecular weight iron species have been detected in the brain in response to cardiac arrest. The increase in iron coincided with an increase in malondialdehyde (MDA) and conjugated dienes during the recirculation period (Krause et al., 1985 Nayini et al., 1985). 

Thyroxine is used in hypothyroidism, a condition that may well present in elderly patients. Side-effects of thyroxine usually occur at excessive doses and include gastrointestinal disturbances (nausea, vomiting) as well as cardiac symptoms such as angina pain, arrhythmias, palpitation and tachycardia. Thyroxine should be used with caution in elderly patients as they are more prone to side-effects. A lower initial dose (25-50 pg daily) is recommended for patients who are over 50 years. Dose adjustments should take place at intervals of at least 4 weeks. A pretreatment electrocardiogram is recommended because changes induced by hypothyroidism (that would be present at baseline) may be confused with ischaemia. 

Myocardial infarction ischaemia in the cardiac muscle leading to necrosis occurring as a result of reduction in coronary blood flow... 

The most prominent effect of halothane on the circulation is a dose-related decrease in arterial blood pressure. This is due mainly to reduced myocardial contractility and ventricular slowing. Cardiac output falls due to a decrease in stroke volume and bradycardia. Systemic vascular resistance also falls but this is less pronounced than with some other agents. Although halothane reduces myocardial oxygen consumption it also reduces oxygen demand and it is suitable for patients with myocardial ischaemia. 

Unlike tubocurarine, pancuronium does not produce ganglionic block or histamine release. For this reason it became popular soon after its introduction and became the drug of choice for use in sick patients. However, it increases the heart rate, arterial pressure, and cardiac output in clinical doses. While this may be advantageous when using high-dose opiate anaesthesia in cardiac surgery, it can be associated with arrhythmias and myocardial ischaemia. The... 

Isoprenaline stimulates pi and 32 adrenoceptors (pi>32) resulting in increased myocardial contractility and reduced peripheral vascular resistance. It does not act on a adrenoceptors. Cardiac output increases partly due to reduced afterload and an increase in heart rate. There is a diversion of blood to non-essential tissues, e.g. skeletal muscle and skin. Because of the decrease in peripheral vascular resistance arterial blood pressure and coronary perfusion pressure may decrease, which may predispose to myocardial ischaemia. 

Hiraishi S, Iwanami N, Ogawa N. Images in cardiology. Enlargement of cardiac rhabdomyoma and myocardial ischaemia during corticotropin treatment for infantile spasm. Heart 2000 84(2) 170. 

Plasma malondialdehyde-like material, an indicator of lipid peroxidation, is increased in conditions of ischaemia, such as stroke [83, 84] and myocardial infarction [85]. Mitochondria extracted from hearts of vitamin-E-deficient rabbits showed a decreased mitochondrial function and an increased formation of oxygen radicals associated with a reduced superoxide dismutase activity. This was partially reversed by addition of vitamin E in vitro [86]. Measurement of in vitro susceptibility to lipid peroxidation in cardiac muscle from vitamin-E-deficient mice showed a highly significant negative correlation between the concentration of vitamin E and in vitro lipid peroxidation. The results indicate that short-term vitamin E deficiency may expose cardiac muscle to peroxidation injuries [ 87 ]. In rats, treatment for 2 days with isoprenaline increased lipid peroxide activity, as measured by malondialdehyde levels, in the myocardium. Vitamin-E-deficient animals were even more sensitive to this effect, and pretreatment with a-tocopheryl acetate for 2 weeks prevented the effect induced by isoprenaline. The authors [88] propose that free-radical-mediated increases in lipid peroxide activity may have a role in catecholamine-induced heart disease. 

The most serious toxic effects of cocaine involve changes in the cardiovascular system. These include cardiac arrhythmias, myocardial ischaemia and infarction, and cerebrovascular spasm, all of which can be largely explained by the facilitation of the action of catecholamines on the cardiovascular system. Another explanation of the cardiotoxicity of cocaine lies in the direct vasoconstrictive properties of its major metabolite, norcocaine. It seems likely... 

Stephanou A, Brar B, Liao Z, Scarabelli T, Knight RA, Latchman DS. Distinct initiator caspases are required for the induction of apoptosis in cardiac myocytes during ischaemia versus reperfusion injury. Cell Death Differ 2001 8 434 135. 

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