Cardiac pacing

Mills P, Michnich M. Managed care and cardiac pacing and electrophysiology. Pacing Clin Electrophysiol 1993 16 1746-50. 

Furthermore, pH determination has been used in other clinical research, both alone and in combination with other measurements. This research includes studies into the relationship between extracellular and intracellular pH in an ischemic heart [6, 7], the pH of airway lining fluid in respiratory disease [8], the study of pH as a marker for pyloric stenosis [9], malnutrition in alkalotic peritoneal dialysis patients [10], pH modulation of heterosexual HIV transmission [11, 12], and wound prevention and treatment [13], In addition, pH changes due to blood acidosis have been used to trigger and pace the ventricular rate of an implanted cardiac pacemaker [14], Research using pH measurements... 

Abstract Two thirds of the nearly half a million deaths per year in the United States due to sudden cardiac death (SCD) is attributed to coronary artery disease (CAD) and most commonly results from untreated ventricular tachyarrhythmias. Patients with ischemic cardiomyopathy and left ventricular dysfunction are at highest risk for SCD, but this still defines only a small subset of patients who will suffer SCD. Multiple lines of evidence now support the superiority of implantable cardioverter defibrillator (ICD) therapy over antiarrhythmic therapy for both primary and secondary prevention of SCD in advanced ischemic heart disease. Optimization of ICD therapy in advanced ischemic cardiomyopathy includes preventing right ventricular pacing as well as the use of highly effective anti-tachycardia pacing to reduce the number of shocks. While expensive, ICD therapy has been shown to compare favorably to the accepted standard of hemodialysis in cost effectiveness analyses. 

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. 

A series of pilot studies began with multisite pacing for patients with heart failure and dilated cardiomyopathy in the early 1990s [52, 105-111]. An improvement in LV function and symptoms of heart failure were demonstrated. This provided the interest in biventricular pacing for heart failure. The term cardiac resynchronization therapy was coined to refer to pacing therapies that attempt to enhance cardiac performance by using pacing to correct electrical conduction abnormalities in the heart. The most common form of this therapy is atrial-synchronous... 

Auricchio A, Sommariva L, Salo RW, Scafuri A, Chiariello L. Improvement of cardiac function in patients with severe congestive heart failure and coronary artery disease by dual chamber pacing with shortened AV delay, [see comment]. Pacing Clin. Electrophysiol. 1993 16 2034 3. 

Rosenqvist M, Bergfeldt L, Haga Y, Ryden J, Ryden L, Owall A. The effect of ventricular activation sequence on cardiac performance during pacing. Pacing Clin. Electrophysiol. 1996 19 1279-86. 

Cazeau S, Bordachar P, Jauvert G, et al. Echocardio-graphic modeling of cardiac dyssynchrony before and during multisite stimulation a prospective study. Pacing Clin. Electrophysiol. 2003 26 137 3. 

Nelson GS, Berger RD, Fetics BJ, et al. Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block, [erratum appears in Circulation 2001 Jan 23 103 (3) 476]. Circulation 2000 102 3053-9. 

Stellbrink C, Breithardt OA, Franke A, et al. Impact of cardiac resynchronization therapy using hemodynami-cally optimized pacing on left ventricular remodeling in patients with congestive heart failure and ventricular conduction disturbances, [see comment]. J. Am. Coll. Cardiol. 2001 38 1957-65. 

Molhoek SG, Van Erven L, Bootsma M, Steendijk P, Van Der Wall EE, Schalij MJ. QRS duration and shortening to predict clinical response to cardiac resynchronization therapy in patients with end-stage heart failure. Pacing Clin. Electrophysiol. 2004 27 308-13. 

Giudici MC, Thornburg GA, Buck DL, et al. Comparison of right ventricular outflow tract and apical lead permanent pacing on cardiac output. Am. J. Cardiol. 1997 79 209-12. 

Fig. 11. Changes In gated NMR spectra during the cardiac cycle. Top panel isovolumic left ventricular pressure In a ferret heart paced at 0.99 Hz in 8 mM [Ca +]. NMR spectra were acquired at the two times indicated on the pressure record (a) 10 ms prior to stimulation (b) 75 ms after stimulation. Middle panel shows gated F NMR spectra (each from 800 acquisitions) recorded at (a) and (b), as indicated. The bound (B) and free (F) peaks of 5F-BAPTA exhibit distinct chemical shifts at approximately 8 and 2 ppm, respectively, downfield from a standard of 1 mM 6-Ftryptophan at 0 ppm. It appears that the free [Ca +] varied during the cardiac cycle. Bottom panel shows gated P spectra (400 scans) acquired at times a and b in the same heart. The major peaks correspond to phosphocreatine (0 ppm), ATP (the three peaks upfield from phosphocreatine), and inorganic phosphate (the small peak at 4-5 ppm) (Reproduced from Marban et al. Circ. Res. 1988 63 673-678 [311] with permission of Lippincott, Williams Wilkins).

There are also plans to deliver a gene therapy product nonsurgicaUy for the treatment of patients with heart failure. In a controlled trial in a pig model of pacing-induced heart failure, intracoronary delivery of human FGF-4 showed significant improvement in regional cardiac function and a reduction in the size of the heart. If these results translate favorably to humans, FGF-4 gene therapy may be a therapeutic option for patients with cardiomyopathy. 

The most frequent cardiovascular effects of an acute overdose are tachycardia and hypotension. The hypotension is partially related to a relative volume depletion, but correction does not bring complete resolution. Even though radionuclide and catheterization studies have shown that TCAs do not impair LVF, either at therapeutic plasma levels or with overdose, data are not available for victims who died. One study describes two cases of fatal overdose in which ventricular pacing produced regular ventricular depolarization but minimal cardiac output, suggesting that at very high concentrations, TCAs might directly impair the myocardium (as demonstrated in animal studies) (429). 

Isoprenaline occasionally has a place in the management of cardiac conditions in which bradycardia is a feature, e.g. low cardiac output associated with slow heart rate after extracorporeal circulation in patients with excessive p-blocking therapy. It may also be used in the treatment of overdose with (3-adrenoceptor antagonists and for refractory bradyarrhythmias prior to cardiac pacing. Isoprenaline is used in the treatment of bronchial asthma on account of its 32 effects. 

Patients with normal sinus rhythm and a wide QRS interval, eg, greater than 120 ms, have impaired synchronization of ventricular contraction. Poor synchronization of left ventricular contraction results in diminished cardiac output. Resynchronization, with left ventricular or biventricular pacing, has been shown to reduce mortality in patients with chronic heart failure who were already receiving optimal medical therapy. 

A 23-year-old woman took chlorpropamide 5-10 g. She needed assisted respiration and cardiac pacing for bradycardia (probably due to blockade of potassium channels), fluid infusion, and forced diuresis for 3 days. Notwithstanding continuous glucose infusion and glucose boluses she relapsed into severe hypoglycemia with convulsions. Only on day 27 was her urine free of chlorpropamide and her blood glucose normal. 

Wu, Y., Bell, S. P., and Trombitas, K. (2002). Changes in titin isoform expression in pacing-induced cardiac failure give rise to increased passive muscle stiffness. Circulation 106, 1384-1389. 

The cardiac arrhythmias are life-threatening, so the patient must be closely monitored, with facilities available for possible resuscitation. Drugs such as quinidine and procainamide are contraindicated, but lidocaine, propranolol, or phenytoin has been used safely and effectively. The arterial blood gas levels, pH, and electrolyte concentrations should be monitored so that metabolic acidosis or hypokalemia can be identified that would further aggravate the arrhythmias. Electrical pacing may be required if the antiarrhythmic drugs fail. Hyperpyrexia is treated by cooling. Seizures may be managed by intravenous doses of diazepam. 

Another novel cardiovascular therapy that has recently come into play is the use of stem cell delivery. These approaches have thus far involved the use of gene delivery mechanisms to essentially force embryonic stem cells into cardiomyocyte differentiation with the goal of producing a cardiac pace-making cell (Arruda et al., 2004). Researchers are also developing methods for utilizing seeded adult mesenchymal stem cells as an implanted base to act as a depot for the delivery of localized gene therapies (Arruda et al., 2004). 

Adverse effects The adverse events associated with (3 blockers may be avoided by starting treatment at very low doses. However, treatment can be associated with complaints of fatigue and weakness, which usually resolve in a few weeks, Sometimes it is necessary to decrease the dose of the (3 blocker or diuretic. Symptomatic bradycardia is another serious adverse effect of (3 blockers, and requires a decrease in the dose or sometimes cardiac pacing to allow the use of this vital medication, Hypotension is another potential side effect however, it is rarely seen as the therapy is started with a very low dose (3,25 mg twice a day for carvedilol, I mg for bisoprolol and 12,5 mg for extended release metoprolol). The administration of ACE inhibitor and diuretic at a different time of day than the (3 blocker can... 

Study Procedure No. of patients FAJ, months or mean SD Death, n (%) Late cardiac mortality, n (%) Acute MI n (%) Ventricular fibrillation, n (%) Permanent pacing, n (%) Reintervention, n (%)... 

Walsh, R. A. (1999). Calcineurin inhibition as therapy for cardiac hypertrophy and heart failure Requiescat in pace Circ. Res. 84, 741-743. 

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