Sudden cardiac deaths

It was hoped that the more complete blockade of angiotensin II s AT effects would confer greater long-term efficacy with ARBs compared to ACE inhibitors. However, prospective, randomized trials suggest that the clinical efficacy of ARBs is similar to that of ACE inhibitors for reduction of hospitalizations for HF, sudden cardiac death, and all cause mortality.23-25 Despite poorer suppression of AT2, comparable efficacy of ACE inhibitors may be due to the additional effects on the kallikrein-kinin system. Although ARBs produce hemodynamic and neurohormonal effects similar to those of ACE inhibitors, they are considered second-line therapy due to the overwhelming clinical trial experience with ACE inhibitors. 

Implantable cardioverter-defibrillators are more effective than antiarrhythmic drugs for reduction in the risk of sudden cardiac death due to VT or VF. 

In patients with underlying CAD or a history of myocardial infarction, the presence of complex or frequent VPDs is associated with an increased risk of mortality due to sudden cardiac death.36... 

Sustained VT requires immediate intervention, because if untreated, the rhythm may cause sudden cardiac death via hemodynamic instability and the absence of a pulse (pulseless VT) or via degeneration of VT into VF. 

The desired outcomes for treatment are to terminate the arrhythmia and restore sinus rhythm, and to prevent sudden cardiac death. 

In some patients, sustained VT results in the absence of a pulse, resulting in the syndrome of sudden cardiac death. 

In patients who have experienced VT and are at risk for sudden cardiac death, implantation of an implantable cardioverter-defibrillator (ICD) is the treatment of choice.44 An ICD is a device that provides internal electrical cardioversion of VT or defibril -lation of VF the ICD does not prevent the patient from developing the arrhythmia, but it reduces the risk that the patient will die of sudden cardiac death as a result of the arrhythmia. Whereas in the past ICD implantation required a thoracotomy, these devices now may be implanted transvenously, similarly to pacemakers, markedly reducing the complication rate. 

ICDs have been found to be significantly more effective than antiarrhythmic agents such as amiodarone or sotalol for reducing the risk of sudden cardiac death 45,46 therefore, ICDs are preferred therapy.44 However, many patients with ICDs receive concurrent antiarrhythmic drug therapy to reduce the frequency with which patients experience the discomfort of shocks and to prolong battery life of the devices. Combined pharmacotherapy with amiodarone and a 3-blocker is more effective than monotherapy with sotalol or (i-blockers for reduction in the frequency of ICD shocks.47... 

Approximately 400,000 people die of sudden cardiac death annually in the United States. While some of these deaths occur as a result of asystole, the majority occur as a result of primary VF or VT that degenerates into VF. Etiologies of VF are presented in Table 6-10 and are similar to those of VT. 

In some patients, torsades de pointes maybe of short duration and may terminate spontaneously. However, torsades de pointes may not terminate on its own, and if left untreated, may degenerate into VF and result in sudden cardiac death.13 Several drugs, including terfenadine, astemizole, and cisapride have been withdrawn from the United States market as a result of causing deaths due to torsades de pointes. 

The desired outcomes for treatment include the (1) prevention of torsades de pointes, (2) termination of torsades de pointes, (3) prevention of recurrence, and (4) prevention of sudden cardiac death. 

Hereditary triose phosphate isomerase (TPI) deficiency is an autosomal recessive disorder that has the most severe clinical manifestations of the erythroenzy-mopathies, including hemolytic anemia, neurological dysfunction, sudden cardiac death, and increased susceptibility to infection. Since the first description by Schneider et al. (S10), more than 25 unrelated families have been reported (Fll). Cases of decreased TPI activities associated with cat cry syndrome and pancytopenia were reported, whereas the correlation between TPI deficiency and these disorders was not clear. Although the degree of anemia is variable, most patients require blood transfusions. Neurological involvement, such as paraparesis, weakness, and hypotonia, is progressive in most cases. No specific therapy is available for the neuropathic manifestations of the disease, and most severely affected children fail to survive beyond the age of 5 years. 

The long-term goals after MI are to (1) control modifiable coronary heart disease (CHD) risk factors (2) prevent development of systolic heart failure (3) prevent recurrent MI and stroke and (4) prevent death, including sudden cardiac death. 

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). 

Blocker (without ISA) and ACE inhibitor therapy is recommended. /J-Blockers decrease cardiac adrenergic stimulation and reduce the risk of a subsequent MI or sudden cardiac death. ACE inhibitors improve cardiac function and reduce CV events after MI. ARBs are alternatives to ACE inhibitors in postmyocardial patients with LV dysfunction. 

Enkaid (4 years on market) Anti arrhythmic Cardiovascular (sudden cardiac death)... 

Los s-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death. Circulation, 115, 442-449. 

Sherief HT, Carpentier RG. (1991). Electrophysiological mechanisms of cocaine-induced cardiac arrest. A possible cause of sudden cardiac death. J Electrocardiol. 24(3) 247-55. 

Approximately 400,000 lives in the United States are claimed each year due to sudden cardiac death (SCD) [1], Most of these deaths are due to an electri-... 

While most -blocking agents on acute administration have little direct electrophysiological effects, studies in rabbits [94] and man [95] have shown that chronic administration of y -blockers increases APD. This increase in APD (and hence refractory period) has been postulated to contribute to the effectiveness of -receptor blocking agents in the prevention of sudden cardiac death [94]. Direct Class III action has been claimed for the y -blockers oxprenolol (30) [96,97], nadolol (31) [96] and atenolol (10) [98] in addition... 

Of greater concern is the safety of the TCAs. Toxic levels of these medications can produce lethal cardiac arrhythmias, seizures, and suppression of breathing. An overdose of a 1-2 week supply of most TCAs is often fatal, a serious consideration when prescribing medication to depressed patients with suicidal thoughts. Children taking imipramine for treatment of ADHD have died from sudden cardiac death consequently, child psychiatrists seldom use TCAs. Likewise, patients with heart disease or seizure disorders are more likely to have dangerous complications from TCAs and should avoid them. 

Exercise is not without risks these include sudden cardiac death, hyperthermia, hypothermia, hypoglycaemia, hypo-natraemia, a reduction in the effectiveness of the immune system, overuse injury and interference in the reproductive system in females. Whether severe physical activity affects the reproductive system in males is sometimes discussed but these are no reports in the scientific literature. 

---