Search PubMedSearch

PubMed · 8656137

Errors in ECG parameter estimation from standard leadsets.

Abstract

With the availability of low-cost, high-speed computers with (relatively) vast amounts of storage has come something of an explosion in the application of "quantitative electrocardiography." A search of the Medline medical reference database on the subject string "quantitative AND electrocardiography" reveals no less than 509 citations, suggesting that the term has gained widespread acceptance. However, while quantitative techniques are, in general, to be welcomed to clinical medicine and research, their use as a diagnostic or patient monitoring tool begs a careful examination of just what is being counted and how it is being linked to physiology. In this study, the authors focus on the use of standard electrocardiographic lead systems as the basis for quantitative patient evaluation and attempt to highlight some limitations in the ability to extract meaningful parameters with such a limited sampling of human thoracic electrical activity.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R S MacLeod, R L Lux. 1995. Errors in ECG parameter estimation from standard leadsets.. https://doi.org/10.1016/s0022-0736(95)80033-6

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Inhibition of intimal thickening after balloon angioplasty in porcine coronary arteries by targeting regulators of the cell cycle.

BACKGROUND: Although percutaneous transluminal coronary angioplasty (PTCA) is a highly effective procedure to reduce the severity of stenotic coronary atherosclerotic disease, its long-term success is significantly limited by the high rate of restenosis. Several cellular and molecular mechanisms have been implicated in the development of restenosis post-PTCA, including vascular smooth muscle cell (VSMC) activation, migration, and proliferation. Recently, our group demonstrated that rapamycin, an immunosuppressant agent with antiproliferative properties, inhibits both rat and human VSMC proliferation and migration in vitro. In the present study, we investigated (1) whether rapamycin administration could reduce neointimal thickening in a porcine model of restenosis post-PTCA and (2) the mechanism by which rapamycin inhibits VSMCs in vivo. METHODS AND RESULTS: PTCA was performed on a porcine model at a balloon/vessel ratio of 1.7+/-0.2. Coronary arteries were analyzed for neointimal formation 4 weeks after PTCA. Intramuscular administration of rapamycin started 3 days before PTCA at a dose of 0.5 mg/kg and continued for 14 days at a dose of 0.25 mg/kg. Cyclin-dependent kinase inhibitor (CDKI) p27(kip1) protein levels and pRb phosphorylation within the vessel wall were determined by immunoblot analysis. PTCA in the control group was associated with the development of significant luminal stenosis 4 weeks after the coronary intervention. Luminal narrowing was a consequence of significant neointimal formation in the injured areas. Rapamycin administration was associated with a significant inhibition in coronary stenosis (63+/-3.4% versus 36+/-4.5%; P<0.001), resulting in a concomitant increase in luminal area (1.74+/-0.1 mm2 versus 3. 3+/-0.4 mm2; P<0.001) after PTCA. Inhibition of proliferation was associated with markedly increased concentrations of the p27(kip1) levels and inhibition of pRb phosphorylation within the vessel wall. CONCLUSIONS: Rapamycin administration significantly reduced the arterial proliferative response after PTCA in the pig by increasing the level of the CDKI p27(kip1) and inhibition of the pRb phosphorylation within the vessel wall. Therefore, pharmacological interventions that elevate CDKI in the vessel wall and target cyclin-dependent kinase activity may have a therapeutic role in the treatment of restenosis after angioplasty in humans.

Angioplasty, Balloon, Coronary

Determinants of stent restenosis in chronic coronary occlusions assessed by intracoronary ultrasound.

Chronic coronary occlusions have a high recurrence rate that can be reduced by stenting, but this rate remains higher than in nonocclusive lesions. To analyze possible determinants of restenosis in these lesions, intracoronary ultrasound was performed during the recanalization procedure. A chronic coronary occlusion of > or = 1 month duration (range 1 to 33 months; median 3.3) was successfully recanalized in 41 patients. Quantitative ultrasound analysis was performed before and after stent placement, with measurement of the luminal area, the extent of the plaque burden at the site proximal and distal to the occlusion, and within the occlusion and the subsequent stent. The degree of compensatory enlargement of the coronary artery within the occlusion was determined by comparing the average of the total vessel area of the proximal and distal reference with the lesion site. Early reocclusion (subacute stent thrombosis) was observed in 1 patient (2.4%). The angiographic control after 6 months showed restenosis in 9 patients with 1 late reocclusion. The overall recurrence rate was 24%. There was no difference in clinical and procedural characteristics between lesions with restenosis and without restenosis. The latter had a larger minimum stent area (7.59 +/- 1.96 mm2 vs 5.71 +/- 0.90 mm2; p <0.01), and there was evidence for more compensatory vessel enlargement in lesions without restenosis. Thus, intracoronary ultrasound showed that a smaller minimum stent area was a major predictor of angiographic restenosis, and it occurred more often in occlusions without compensatory vessel enlargement.

Angioplasty, Balloon, Coronary