Myocardial abnormalities

Although the history, physical examination, and laboratory tests can provide important clues to the underlying cause of heart failure, imaging is required to identify any structural abnormality of the heart. In most patients, an echocardiogram is used to detect any valvular, pericardial, or myocardial abnormalities. The echocardiogram also can determine the presence of systolic and/or diastolic dysfunction and the left ventricular ejection fraction (LVEE). 

Additionally, the electrophysiological effects are often obtained from normal myocardial preparations and the abnormalities of cellular electrophysiology which cause arrhythmias in a diseased myocardium may be uniquely related to the disease process (10). Nevertheless, antiarrhythmic agent classifications have been useful as a mnemonic device. 

It is well accepted that hypertension is a multifactorial disease. Only about 10% of the hypertensive patients have secondary hypertension for which causes, ie, partial coarctation of the renal artery, pheochromacytoma, aldosteronism, hormonal imbalances, etc, are known. The hallmark of hypertension is an abnormally elevated total peripheral resistance. In most patients hypertension produces no serious symptoms particularly in the early phase of the disease. This is why hypertension is called a silent killer. However, prolonged suffering of high arterial blood pressure leads to end organ damage, causing stroke, myocardial infarction, and heart failure, etc. Adequate treatment of hypertension has been proven to decrease the incidence of cardiovascular morbidity and mortaUty and therefore prolong life (176—183). 

These dm are primarily used in the treatment of hypertension (see the Summary Drug Table Adrenergic Blocking Drugs also see Chap. 39) and certain cardiac arrhythmias (abnormal rhythm of the heart), such as ventricular arrhythmias or supraventricular tachycardia They are used to prevent reinfarction in patients with a recent myocardial infarction (1—4 weeks after MI). Some of these dm have additional uses, such as the use of propranolol for migraine headaches and nadolol for angina pectoris. 

Hypertrophic cardiomyopathy (HCM) is characterized by abnormal left ventricular thickening. The left ventricular septum is the most common site of involvement. Pathologically, the disease is characterized by myocardial fiber disarray. The myocardium may exhibit extensive scarring and disorganization of interstitial and intercellular tissue (Elstein et al., 1992). The severity of HCM depends on the age of the patient, as well as the extent of the disarray. Patients with HCM have variable... 

Inherited Cardiomyopathies Are Due to Disorders of Cardiac Energy Metabolism or to Abnormal Myocardial Proteins... 

Abnormalities of myocardial contractile and structural proteins P-Myosin heavy chains, troponin, tropomyosin, dystrophin... 

LD isoenzyme abnormality does not precede the appearance of the (mb) in the serum following myocardial infarction. The reappearance of (mb) is interpreted as diagnostic of reinfarction, and correlates with new electrocardiographic changes and an altered clinical course. 

Electrocardiogram (ECG) May be normal or could show numerous abnormalities including acute ST-T-wave changes from myocardial ischemia, atrial fibrillation, bradycardia, and LV hypertrophy. 

Ventricular premature depolarizations occur as a result of abnormal ventricular automaticity, as a result of enhanced activity of the sympathetic nervous system and altered electro-physiologic characteristics of the heart during myocardial ischemia and following myocardial infarction. 

Structural abnormalities such as atrial-septal aneurysm Myocardial infarction... 

Cardiovascular Cardiomegaly, myocardial ischemia, murmurs, and abnormal electrocardiogram patients with SCD have... 

Ventricular tachycardia (VT) is defined by three or more repetitive PVCs occurring at a rate greater than 100 beats/min. It occurs most commonly in acute myocardial infarction (MI) other causes are severe electrolyte abnormalities (e.g., hypokalemia), hypoxemia, and digitalis toxicity. The chronic recurrent form is almost always associated with underlying organic heart disease (e.g., idiopathic dilated cardiomyopathy or remote MI with left ventricular [LV] aneurysm). 

Deficiency of vitamin E is rare it can occur from abnormalities in lipid absorption as well as dietary deficiency. Its deficiency affects the muscular system, causing dystrophy and paralysis and, if the heart is affected, death by myocardial failure. This is probably caused by demyelin-ation of axons due to oxidative damage. Vitamin E is incorporated into chylomicrons within the enterocyte, so that its uptake into cells requires the activity of lipoprotein lipase. 

Sinus bradycardia. An abnormally low sinoatrial impulse rate (<60/min) can be raised by parasympatholytics. The quaternary ipratropium is preferable to atropine, because it lacks CNS penetrability (p. 107). Sympathomimet-ics also exert a positive chronotropic action they have the disadvantage of increasing myocardial excitability (and automaticity) and, thus, promoting ectopic impulse generation (tendency to extrasystolic beats). In cardiac arrest epinephrine can be used to reinitiate heart beat... 

Renal disease or renal dysfunction (eg, as suggested by serum creatinine levels greater than or equal to 1.5 mg/dL [males], greater than or equal to 1.4 mg/dL [females], or abnormal Ccr) that may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction (Ml), and septicemia CHF requiring pharmacologic treatment hypersensitivity to metformin acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Treat diabetic ketoacidosis with insulin. 

Sdringola S, Nakagawa K, Nakagawa Y, Yusuf SW, Boccalandro F, Mullani N et al. Combined intense lifestyle and pharmacologic lipid treatment further reduce coronary events and myocardial perfusion abnormalities compared with usual-care cholesterol-lowering drugs in coronary artery disease. J Am Coll Cardiol 2003 41 263-272... 

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. 

Although much of the data regarding the frequency of conduction abnormalities during acute myocardial infarction were derived from studies prior to the era of rapid reperfusion [14 17], data from more recent trials suggest that the incidence of intraventricular conduction defects has changed very little. 

Evidence-based pharmacotherapy provides a succinct appreciation of the benefits of a drug, but rarely takes into account the patient s quality of life. Eor instance, intensive statin therapy is recommended because it reduces the incidence of cardiovascular death (odds ratio 0.86), myocardial infarction (odds ratio 0.84), and stroke (odds ratio 0.82) however, the increased risks for any adverse event (odds ratio 1.44), for abnormalities on liver function testing (odds ratio 4.48), for elevations in CK (odds ratio 9.97) and for adverse events requiring discontinuation of therapy (odds ratio 1.28) are less often taken into account by the prescriber. This example emphasises that individualisation is of the utmost importance to keep an acceptable benefit/risk ratio (Clin Ther 2007 29 253-60). The benefits of evidence-based pharmacotherapy may be obtained whenever concordance/compliance of the patient is adequate. However, concordance rate is slightly higher than 30% for chronic conditions, such as hypertension (Curr Hypertens Rep 2007 9 184-9), indicating that the patient has to be educated about the use of drugs, and therapy has to be individualised. 

A considerable body of literature supports abnormalities in myocardial excitation-contraction couphng in CHF. An appreciation of the principles involved in this cell signaling process is crucial to understand current and future pharmacotherapies for CHF. A brief overview of myocardial excitation-contraction coupling will be provided. 

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