Talk:Cardiovascular System - Heart Rate Development: Difference between revisions

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Valvulogenesis is an extremely complex process by which a fragile gelatinous matrix is populated and remodelled during embryonic development into thin fibrous leaflets capable of maintaining unidirectional flow over a lifetime. This process occurs during exposure to constantly changing haemodynamic forces, with a success rate of approximately 99%. Defective valvulogenesis results in impaired cardiac function and lifelong complications. This review integrates what is known about the roles of genetics and mechanics in the development of valves and how changes in either result in impaired morphogenesis. It is hoped that appropriate developmental cues and phenotypic endpoints could help engineers and clinicians in their efforts to regenerate living valve alternatives.
Valvulogenesis is an extremely complex process by which a fragile gelatinous matrix is populated and remodelled during embryonic development into thin fibrous leaflets capable of maintaining unidirectional flow over a lifetime. This process occurs during exposure to constantly changing haemodynamic forces, with a success rate of approximately 99%. Defective valvulogenesis results in impaired cardiac function and lifelong complications. This review integrates what is known about the roles of genetics and mechanics in the development of valves and how changes in either result in impaired morphogenesis. It is hoped that appropriate developmental cues and phenotypic endpoints could help engineers and clinicians in their efforts to regenerate living valve alternatives.


PMID: 17569640
PMID 17569640


http://www.ncbi.nlm.nih.gov/pubmed/17569640
==1997==
 
===Cardiotocogram compared to Doppler investigation of the fetal circulation in the premature growth-retarded fetus: longitudinal observations===
Ultrasound Obstet Gynecol. 1997 Mar;9(3):152-61.
 
Hecher K, Hackelöer BJ.
Source
Department of Prenatal Diagnosis and Therapy, AK Barmbek, Hamburg, Germany.
 
Abstract
 
It was our objective to compare computerized fetal heart rate analysis with blood flow velocity waveform analysis of the arterial and venous fetal circulation in intrauterine growth retardation. We report five illustrative cases with longitudinal observations of fetal Doppler findings and fetal heart rate between 23 and 32 weeks of gestation. Blood flow waveforms were recorded from the umbilical artery, middle cerebral artery, descending aorta, ductus venosus and inferior vena cava. Fetal heart rate was analyzed by a computer system according to the Dawes-Redman criteria. The time sequence of deterioration is described individually for each fetus. An abrupt increase in pulsatility of ductus venosus waveforms with loss of forward flow velocity during atrial contraction preceded abnormally low short-term variation of fetal heart rate. With advanced gestational age and concomitant maternal disease, we observed severe alterations of flow velocity waveforms within 12 h of normal Doppler measurements, which is in contrast to findings in the second trimester, in which severely abnormal venous waveforms were observed over a period of several weeks before intrauterine death occurred. In a fetus with terminally low short-term variation, normal venous waveforms indicated fetal well-being despite an abnormal cardiotocogram (CTG). We challenge the current concept that the CTG is the best available parameter to determine the optimal time for elective delivery of premature growth-retarded fetuses. Deterioration in ductus venosus blood flow seems to precede an abnormal CTG and thus heralds the need for delivery.
 
PMID 9165678

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Fetal Heart Rate

<pubmed limit=10>Fetal Heart Rate</pubmed>

2012

Admission cardiotocography: Its role in predicting foetal outcome in high-risk obstetric patients

Australas Med J. 2012;5(10):522-7. doi: 10.4066/AMJ.2012.1267. Epub 2012 Oct 31.

Rahman H, Renjhen P, Dutta S, Kar S. Source Department of Obstetrics & Gynaecology, Sikkim Manipal Institute of Medical Sciences, Gangtok, India.

Abstract

BACKGROUND: Routine and continuous electronic monitoring of foetal heart rate (FHR) in labour has become an established obstetric practice in high-risk pregnancies in industrialised countries. However, the same may not be possible in non-industrialised countries where antenatal care is inadequate with a large number of high-risk pregnancies being delivered in crowded settings and inadequate health care provider to patient ratios. AIMS: The objective of this study was to evaluate the predictive value of the admission cardiotocogram (CTG) in detecting foetal hypoxia at the time of admission in labour and to correlate the results of the admission CTG with the perinatal outcome in high-risk obstetric cases. METHOD: This was a prospective observational study conducted in the labour and maternity ward of a hospital in Gangtok, India, during the period 2008 to 2010. The study included high-risk pregnant women, admitted via the emergency or outpatient department with a period of gestation ≥36 weeks, in first stage of labour with foetus in the cephalic presentation. All women were subjected to an admission CTG, which included a 20 minute recording of FHR and uterine contractions. RESULTS: One hundred and sixty patients were recruited. The majority of women were primigravida in the 21-30 years age group. About 42% patients were postdated pregnancy followed by pregnancy-induced hypertension (PIH) (15.6%) and premature rupture of membranes (PROM) (11.3%) as the major risk factors. The admission CTG were 'reactive' in 77%, 'equivocal' in 14.4% and 'ominous' in 8.7% women. Incidence of foetal distress, moderate-thick meconium stained liquor and neonatal intensive care unit (NICU) admission was significantly more frequent among patients with ominous test results compared with equivocal or reactive test results on admission. Incidence of vaginal delivery was more common when the test was reactive. CONCLUSION: The admission CTG appears to be a simple non-invasive test that can serve as a screening tool in 'triaging' foetuses of high-risk obstetric patients in non-industrialised countries with a heavy workload and limited resources.

PMID 23173014

2010

Embryology of the conduction system for the electrophysiologist

Indian Pacing Electrophysiol J. 2010 Aug 15;10(8):329-38.

Mirzoyev S, McLeod CJ, Asirvatham SJ.

Mayo Medical School. Abstract

It is critical for interventional electrophysiologists to thoroughly appreciate the topographic and developmental anatomy of the heart and its conduction system. Not only is understanding cardiac anatomy important to prevent complications from collateral damage and to help guide catheter placement, but developmental anatomy allows a deeper appreciation of the arrhythmogenic substrate. In this article, we briefly review the relevant stages of cardiac development for electrophysiologists. The potential location of normal and abnormal conduction patterns resulting from heterogeneous developmental origin is discussed.


During cardiogenesis, myocytes develop into either contractile or conduction cells. Three models have been proposed by which cardiac cells develop and differentiate [1].

  1. The first model has been traditionally adopted by electrophysiologists and is based on a multiple ring theory. It hypothesizes that during heart chamber development and growth, cells in certain regions of the heart tube do not proliferate as rapidly as cells in genetically predetermined atrial and ventricular regions. As the tubular heart grows, the slower-proliferating myocytes form constrictions or rings around which the heart will fold.
  2. A second recruitment model is based on the idea that the conduction system framework is present in early development and enables recruitment of adjacent myocytes to form further elements of the conduction system.
  3. The third model, the early specification model, postulates that myocytes begin expressing either conduction genes or working (contractile) genes early in the development. Cells expressing conduction system markers slowly proliferate and form components of the conduction system, whereas cells lacking the markers proliferate faster and develop into contractile tissue.


PMID: 20811536 http://www.ncbi.nlm.nih.gov/pubmed/20811536

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2922875/?tool=pubmed


Development of the cardiac conduction system: why are some regions of the heart more arrhythmogenic than others?

Circ Arrhythm Electrophysiol. 2009 Apr;2(2):195-207.

Christoffels VM, Moorman AF.

Heart Failure Research Center, Academic Medical Center, 1105 AZ, Amsterdam, The Netherlands.

PMID: 19808465 http://www.ncbi.nlm.nih.gov/pubmed/19808465

http://circep.ahajournals.org/cgi/content/full/2/2/195

Evaluation of the embryonic and foetal heart rate at 6(+0) to 11(+6) weeks of gestation

Hamela-Olkowska A, Wiech K, Jalinik K, Zaryjewski D, Kornatowski L, Dangel J. Ginekol Pol. 2009 Mar;80(3):188-92. Polish. PMID: 19382610

"RESULTS: FHR varied between 47 and 192 bpm (mean 154 +/- 26 bpm). At 6 weeks, mean EHR was 116 +/- 21 bpm, then slowly increased, reaching mean 172 +/- 9 bpm at 10 weeks. At 11 weeks the mean FHR achieved the level of 165 +/- 7 bpm. The difference was statistically significant. The r-correlation ratio between FHR and the gestational week was 0.58. In case of 7 embryos (2.75%) at 6.1 to 8.1 weeks of gestation slow FHR was noted (< 100 bpm). The scan performed 7-10 days later revealed miscarriages in all cases. CONCLUSIONS: EHR and FHR in the first trimester depends on gestational week. It increases since 6 to 9 weeks and decreases after 10 weeks. The highest values of FHR are observed between 9 and 10 weeks of gestation. The risk of early pregnancy loss increases significantly in case of detecting slow FHR. FHR can be checked by M-mode methods using any kind of ultrasound machine."


Valvulogenesis: the moving target

Philos Trans R Soc Lond B Biol Sci. 2007 Aug 29;362(1484):1489-503.

Butcher JT, Markwald RR.

Department of Biomedical Engineering, 270 Olin Hall, Cornell University, Ithaca, NY 14853, USA. jtb47@cornell.edu Abstract Valvulogenesis is an extremely complex process by which a fragile gelatinous matrix is populated and remodelled during embryonic development into thin fibrous leaflets capable of maintaining unidirectional flow over a lifetime. This process occurs during exposure to constantly changing haemodynamic forces, with a success rate of approximately 99%. Defective valvulogenesis results in impaired cardiac function and lifelong complications. This review integrates what is known about the roles of genetics and mechanics in the development of valves and how changes in either result in impaired morphogenesis. It is hoped that appropriate developmental cues and phenotypic endpoints could help engineers and clinicians in their efforts to regenerate living valve alternatives.

PMID 17569640

1997

Cardiotocogram compared to Doppler investigation of the fetal circulation in the premature growth-retarded fetus: longitudinal observations

Ultrasound Obstet Gynecol. 1997 Mar;9(3):152-61.

Hecher K, Hackelöer BJ. Source Department of Prenatal Diagnosis and Therapy, AK Barmbek, Hamburg, Germany.

Abstract

It was our objective to compare computerized fetal heart rate analysis with blood flow velocity waveform analysis of the arterial and venous fetal circulation in intrauterine growth retardation. We report five illustrative cases with longitudinal observations of fetal Doppler findings and fetal heart rate between 23 and 32 weeks of gestation. Blood flow waveforms were recorded from the umbilical artery, middle cerebral artery, descending aorta, ductus venosus and inferior vena cava. Fetal heart rate was analyzed by a computer system according to the Dawes-Redman criteria. The time sequence of deterioration is described individually for each fetus. An abrupt increase in pulsatility of ductus venosus waveforms with loss of forward flow velocity during atrial contraction preceded abnormally low short-term variation of fetal heart rate. With advanced gestational age and concomitant maternal disease, we observed severe alterations of flow velocity waveforms within 12 h of normal Doppler measurements, which is in contrast to findings in the second trimester, in which severely abnormal venous waveforms were observed over a period of several weeks before intrauterine death occurred. In a fetus with terminally low short-term variation, normal venous waveforms indicated fetal well-being despite an abnormal cardiotocogram (CTG). We challenge the current concept that the CTG is the best available parameter to determine the optimal time for elective delivery of premature growth-retarded fetuses. Deterioration in ductus venosus blood flow seems to precede an abnormal CTG and thus heralds the need for delivery.

PMID 9165678