Left ventricular stimulation

McVenes R. The future of left ventricular stimulation Transvenous, endocardial or epicardial (Abstract). Europace 2002 3 A13. 

The progenitor cells of the kidney produce 90% of the hormone erythropoietin (EPO), which stimulates red blood cell (RBC) production. Reduction in nephron mass decreases renal production of EPO, which is the primary cause of anemia in patients with CKD. The development of anemia of CKD results in decreased oxygen delivery and utilization, leading to increased cardiac output and left ventricular hypertrophy (LVH), which increase the cardiovascular risk and mortality in patients with CKD. 

Doshi RN. The left ventricular-based cardiac stimulation post av nodal ablation evaluation study. New Orleans, LA American College of Cardiology Annual Scientific Sessions, 2004. 

Gold MR, Auricchio A, Hummel JD, et al. Comparison of stimulation sites within left ventricular veins on the acute hemodynamic effects of cardiac resynchronization therapy. Heart Rhythm 2005 2 376-81. 

Kang HJ, Kim HS, Zhang SY, Park KW, Cho HJ, Koo BK, Kim YJ, Soo Lee D, Soon DW, Han KS, Oh BH, Lee MM, Park YB. Effects of intracoronary infusion of peripheral blood stem-cells mobilised with granulocyte-colony stimulating factor on left ventricular systolic function and restenosis after coronary stenting in myocardial infarction the MAGIC cell randomised clinical trial. Lancet 2004 363 751-756. 

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).

Cardiovascular system. Both caffeine and theophylline directly stimulate the myocardium and cause increased cardiac output, tachycardia and sometimes ectopic beats and palpitations. This effect occurs almost at once after i.v. injection and lasts half an hour. Theophylline contributes usefuUy to the relief of acute left ventricular failure. There is peripheral (but not cerebral) vasodilatation due to a direct action of the drugs on the blood vessels, but stimulation of the vasomotor centre tends to counter this. Changes in the blood pressure are therefore somewhat unpredictable, but caffeine 250 mg (single dose) usually causes a transient rise of blood pressure of about 14/10 mmHg in occasional coffee drinkers (but has no additional effect in habitual drinkers) this effect can be used advantageously in patients with autonomic nervous system failure who experience postprandial hypotension (2 cups of coffee with breakfast may suffice for the day). In occasional coffee drinkers 2 cups of coffee (about 160 mg caffeine) per day raise blood pressure by 5/4 mmHg. Increased coronary artery blood flow may occur but increased cardiac work counterbalances this in angina pectoris. 

Morphine, by a central action, impairs sympathetic vascular reflexes (causing veno- and arteriolar dilatation) and stimulates the vagal centre (bradycardia) it also releases histamine (vasodilatation). These effects are ordinarily unimportant, but they can be beneficial in acute left ventricular failure, relieving mental distress by tranquillising, cardiac distress by reduction of sympathetic drive and preload (by venodilatation), and respiratory distress by rendering the centre insensitive to afferent stimuli from the congested lungs. 

Cirrhotic cardiomyopathy This term is defined as a left ventricular functional disorder due to stress (e. g. hyperdynamic circulation) or as pharmacological stimulation. But also the possibility of (toxically induced ) subclin-ical myocardial damage is discussed, especially because elevated troponin 1 serum values are detectable in every third patient. (81, 142, 187) (Troponin is connected with propomyosin in the actin filaments at regular intervals and, as a relaxing protein , has an important function in muscle metabolism, also in the heart). 

Hypertension, with or without simultaneous hypertrophic myopathy, is a common feature of adrenal stimulation that seems to be common with depot tetracosactide but not simple tetracosactide (3). During treatment for infantile spasms, hypertension occurred more often in those treated with high doses (SEDA-19, 374) (4), and changes in cardiac function, such as left ventricular shortening fraction, can occur early and sometimes before systolic hypertension (SEDA-19, 374) (5). 

Hypertension accelerates atherosclerosis and stimulates left ventricular and vascular hypertrophy. These pathologic changes are thought to be secondary to both a chronic pressure overload and a variety of nonhemodynamic stimuli. Some of the nonhemodynamic disturbances that have been implicated in these effects include the adrenergic system, RAAS, increased synthesis and secretion of en-dothelin I, and a decreased production of prostacyclin and nitric oxide. Accelerated atherogenesis in hypertension is accompanied by proliferation of smooth muscle cells, lipid infiltration into the vascular endothelium, and an enhancement of vascular calcium accumulation. 

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