Cardiac Function - Science topic
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I'm referring to the overlapping sigmoidal curves that are used to describe the gain-of-function mechanisms. I understand the activation curve, but I can't seem to get my head around the inactivation curve. Any help at all would be very much appreciated, whether that is an explanation or pointing to one in the literature. It would also be helpful if you could explain the holding potential, depolarising voltage steps, and pre-pulse vs test pulse. Thank you in advance!
Can I use EDPVR to characterize LV compliance if I get that EDPVR from PV loop at steady state, without loading change? What are the limitation of this indice?
Premise 1: Neurogenic bradycardia and RSA are mediated by different branches of the vagus and need not respond in concert.
Premise 2: Neurogenic bradycardia associated with orienting is a phylogenetic vestigial relic of the reptilian brain and is mediated by the dorsal motor nucleus (DMNX).
Premise 3: Withdrawal of cardiac vagal tone through Nucleus Ambiguus (NA) mechanisms is a mammalian adaptation to select novelty in the environment while coping with the need to maintain metabolic output and continuous social communication.
(From Porges SW (2013) Polvagal Theory. NY: Norton)
The current evolutionary vagal evidence indicates that neither Premises 2 nor 3 are accurate. Also 1) there is a confluence of evidence regarding Premise 1 showing that the DMNX may only manifest vagal effects upon heart rate under conditions of severe physiological respiratory distress (and even this is not very well documented), 2) Porges provides merely very indirect findings to support his hypothesis (and his Figure 2.3 of the time course of putative DMNX-stimulated bradycardia in a single anesthetized rabbit shows much too rapid onset and offset for the heart rate drop to be a response of the unmyelinated DMNX vagal fibers [which should have a much more gradual onset and offset than shown because slow conduction time of these fibers prevent sudden changes]), and 3) no mention is made by Porges of earlier findings that indicate that the DMNX is not implicated in normal vagal control of heart rate.
Nevertheless, perhaps there are strands of direct evidence of which I am unaware? In any case, polvagal conjectures have become very popular in psychology, psychophysiology and therapy literature. It seems, therefore, high time to critically assess the value of Stephen Porges' ideas in this area.
I am working on rat's isolated hear using langendorff system. I apply a specific heart rate of 310 bpm and measure parameters such as: Left ventricle pressure (LVP), perfusion pressure (PP), and Developed pressure (DP).
I have a recurrent problem which is the apparition of ectopic heart which affect the signal DP and LVP. These ectopic peaks are quiet frequent, thought inconsistent. Their superimposition to the normal signal give a noisy look to the graphs and when I test a drugs, the response seem to be lost because of this significant noise.
Attached document is a picture of an original chart taken at different zooms.
Anybody has already experiment that?
Any explanations and suggestion to fix this problem?
You help will be greatly appreciate
We would like to use the GRACE RISK SCORE in our myocardial infarction registry. Does anybody knows the formula or has a syntax to compute the GRACE SCORE?
James A. Reiffel presented an enigmatic ECG (Circulation. 2016;134:499. DOI: 10.1161/CIRCULATIONAHA.116.023662)
The patient is a 52-year-old male corporate executive who comes to the office as a new patient, having just been relocated by his company. He gives a histy of smoking (1 pack per day for 25 years), hyperlipidemia, and hypertension, and he currently is taking a statin, an angiotensin receptor blocker, a β-blocker, and a daily aspirin. He denies any history of chest pain or dyspnea, other than 2 days of mild chest fullness with slight shortness of breath 2 months earlier during a vacation to Vail, Colorado, after a particularly stressful period at work. On return home, he saw his internist who told him, after obtaining a confirmatory echocardiogram, that he had experienced a myocardial infarction, but that his heart function was near normal. At that time, his medications were adjusted to his current regimen. He has no previous medical records with him, but denies any other recent or remote illnesses. An ECG is obtained and is shown (Figure below). What is your interpretation?
i am working for prediction of casualties by heart diseases through ECG signals (HRV analysis). it would be helpful if experts in this field suggest for what kind of HRV changes are observed for any abnormal activity by the heart.
How can we preserve the isolated heart preparation for twenty four hours?
Can someone explain the molecular level signalling pathways of this phenomenon?
When we perform staining for alpha actinin in rat cardiomyocytes we see difference in the sacromere organization. Somewhere it is diffused, somewhere they are perfectly organized with clearly visibly striations. Which is sign for normal healthy cardiac functional cells. Could a highly aligned sarcomere be any link to hypertrophy?
What will happen to the pressure in the ball (image shown) with four different types of pumping mechanics? Can it be related with heart rate and blood pressure, so that the influence of heart rate and strength of cardiac contraction be seriously taken into account in understanding individual-specific blood pressure?
I'm working on detecting different fragments of cardiac Troponin I (Not using a kit) in the patients' sera of different cardiac diseases.
I'm using the best antibodies recommended by Hytest (19c7 for capture, and 560, M18, and MF4 for detection, each at a time), papers indicate that those antibodies can detect down to 0.052 ng/mL, but I can't get them to work!!!!
I use the international human troponin standard for my standard curve.
The M18 gives the best reading with the serial dilutions down to 0.3 ng/mL in the best days, but the other two always gave me worse results (like reading only to 1 ng/mL).
Now, we bought new 560 and MF4 which are a lot worse. This could be an affinity issue, but what was published is very different from my results, they hardly detect down to 2.5 ng/mL !!
I usually biotinylate the detection antibodies myself with a biotinylation kit, then test them right after , even before aliquoting, and they worked fine for the first time.
After aliquoting, I directly incubated them in a serial dilution, compared them to my previously used M18, they were fine, BUT as soon as I started incubating my troponin in serial dilutions, they are 100 times weaker less sensitive, tried the whole sandwich experiment (incubating the capture), and the results were even worse.
For some reason, I can't get them to work as I did in the first time. Could they be degrading? I don't think so, as I'm adding azide to 0.1% as the manufacture suggested.
I prepare fresh buffers, didn't get any better.
Increased their concentration to 10 ug/mL, got a bit better but not even close to my previous results (I usually use both the detection and the capture at 2 ug/mL)
To me, I'm using the best components, can't get the expected results (which I got previously)
Can someone help ?
I'm trying to isolate cardiac fibroblasts from pig and rat hearts but all the protocols I've been trying seems to not work quite well. I do have some fibroblasts, but too few for the amount of tissue I'm using (I'm able to get one or two wells of a 12-well plate for every 20g of tissue).
So, in your experience, what is the best protocol for cardiac fibroblast isolation?
I was wondering if really there is any direct evidence indicating that the generation of early afterdepolarizations (EADs) in the cardiac myocytes causes arrhythmias (e.g. Torsades de pointes and ventricular fibrillation).
Specifically: Deceleration of left ventricular contraction during systole produces an expansion pressure wave (pressure drop) just before valve closure. Is it conceivable that (under possibly pathological condition) the timing of the expansion wave may modulate the radial pulse pressure wave form (incident and reflected wave) into a type-C pressure wave form (wave forms according to Murgo et al. and Nichols et al.)? Is it possible that a pathological condition may thereby produce a radial waveform which is typically associated with a healthy CV system? Has anybody made such observation in practice?
The parameters to be analyzed in my research are
Can you explain if it is worth to buy Polar RS800CX to get practical recording or Suunto t6 HRM?
Even though plasma Ang II levels are determined by plasma renin activity regulated by JG cells, levels of hepatic angiotensinogen production, and pulmonary ACE activity, can ACE and AT1R mRNA expression in the myocardium be used to determine Ang II regulation?
any possible interaction between arrhythmia and heart scan results?
I'm currently researching on left ventricle motion quantification. Can anyone suggest me any heart or left ventricle localization method in tagged cardiac MRI images? Appreciate if you can provide me references too. Thanks.
Type 2 CRS is defined as renal detoriation due to chronic heart failure. because of chronic fluid overload due to CHF, renal venose pressure is increased. thus glomerular filtration rate is decreased. if we use of dopamine in 2 mg/kg/min dosage, afferent arteriol would dilated and GFR would be increased. Is it like this indeed? is there anyone who had experience use of dopamine (2 mg/kg/min) in Type 2 Cardio Renal Syndrome?
Although the association of HR and outcome is suggestive, it does not, by itself, prove causality. High HR also is associated with poor cardiorespiratory fitness or impaired cardiac function. Indeed, exercise capacity itself is a powerful predictor of mortality, and resting HR is lower in individuals who undertake vigorous leisure activities or participate in sports. Therefore, in recent studies significantly relating HR and mortality, adjustments have been made for the effects of physical activity and cardiac function. In the Cooper Clinic Mortality Risk Index, high HR and low cardiorespiratory fitness were both independent predictors of mortality. Relatively high HR often is found together with other cardiovascular risk factors, notably hypertension, an atherogenic blood lipid profile, blood glucose and insulin levels, and overweight. Indeed, HR correlates with the number of cardiovascular risk factors presenting in an individual.
While generating PV loops for cardiac function analysis, I take baseline values and perform VCI occlusion. I also get load-independant parameters under baseline conditions (ESPVR, EDPVR etc). Can I use these also for the data analysis or are these values only valid after VCI occlusion?
Muscle-derived signals involved in the control of local circulation are intimately involved in the coupling of muscle blood flow and cardiac output.
Seeking to develop a dysrhythmic heart failure model specifically for an EP corrective method.
ECHO is not raccomended in the guidelines for CRT selection, but in many centers still has a role especially in borderline situations
Slow flow coronaries are seen on the angio's of many cases of chest pain, and especially those with hyperlipidaemia.
Both the EVEREST II high-risk registry and the European experience (Franzen and Tamburino) enrolled patients with FE not less than 20%.
Deleting the volume overload secondary to severe mitral regurgitation in patients with severe left ventricular dysfunction could have a negative impact.
I have evaluated cardiotonic activity of one herb, at that time I used Langendorff's apparatus. I also checked the intracellular (myocyte) Ca2+ level. But I want to know that is there any other technique by which we can check the change in force of contraction of heart?
I have a 65-year-old female with metallic aortic valve on warfarin, presented with dense left sided hemiplegia. Brain CT showed massive right hemisphere infarction. The patient admitted to the ward as a stroke attributed to valvular lesion. The cardiologist strongly recommends continuing warfarin to prevent further thromboembolic showering and to prevent valve dysfunction, while the neurologist strongly recommends holding warfarin as the risk of intra-infarct bleeding is high. In view of these two contradictory opinions, how would I manage this case? I need experts’ opinion