pacemaker cells and myocardial cells

I read today that skin cells have been turned into myocardial cells. This means obviously, no rejection problems. The success has been shown in rats and is a few years from human use, but it does look promising. This is obviously a brilliant treatment for heart failure, but in all cases? If heart failure is caused by ischemia, and I think ultimately a high proportion are, then how will this help?

Angina is an equivalent of a muscle cramp, meaning there is low blood flow, but there isn't complete block of flow. The cells are starving for oxygen and nutrients during that time but they aren't dying or getting damaged because angina is mostly felt during exertion and it resolves with resting. A heart attack is the most extreme type of blood flow limitation where the muscle cells arent' getting any blood flow and they are beginning to die.

The ST segment can become either depressed or elevated for ventrical receiving an insufficient supply of blood and/ or the heart cells are difficient of oxygen (hypoxia). , QUOTE: is transmural mi is called q wave mi definitely? is transmural mi is called q wave mi definitely? >>>>>The presence of the Q wave in the absence of ST and T wave abnormality generally indicates prior or healed infarction.

) of vessel blood flow to cause cell necrosis (death), but there is a window of opportunity of a few hours to provide oxygen to heart cells that are only stunned and can sometimes be revitalized..

This allows the pacemaker cells within the SA node to be in control of generating and pacing the heartbeat. But, if a particular group of cells in areas remote from the SA node become extra- or hyper-excitable they can take over as the pacemaker for one or several beats, or for a longer term. You might think of the heart's cells as a schoolyard full of young boys playing soccer. Some are inherently quick and fast and are always on top of the game, while others usually play a little slower.

If there is a connection with anomalous RCA and pericarditis, the connection would most likely be due to myocardial infarction (damaged heart cells). The damaged heart cells can be due to ischemia (lack of blood flow) caused by the RCA anomaly.

They are released into the bloodstream with myocardial injury. They are highly specific for myocardial injury--more so than CK-MB--and help to exclude elevations of CK with skeletal muscle trauma. Troponins will begin to increase following MI within 3 to 12 hours, about the same time frame as CK-MB. However, the rate of rise for early infarction may not be as dramatic as for CK-MB. . Creatine kinase can be further subdivided into three isoenzymes: MM, MB, and BB.

Electrical cells make up the conduction system of the heart and are distributed in an orderly fashion (pathways) through the heart. They are specific cells to automatically generate and discharge an electrical impulse. Conductivity – the ability to transmit an electrical impulse from one cell to the next the ability of the cell to respond to an electrical impulse.

I recently had 23 MILLION STEM CELLS injected into my heart via an angiogram. 80% were dedicated to grow new heart tissue and 20% were "rogue" type cells put into my vascular system. These were stem cells made from my OWN STEM CELLS not embryonic. So, no chance of rejection, no extra pills to take. There is over an 80% chance of improvement. My EF was between 12 and 15% before new stem cells. Have not had another EF test yet. I am diabetic(insulin dependent.

Usually, the heart muscle cells keep time more slowly than normal pacemaker cells. This allows the pacemaker cells within the SA node to be in control of generating and pacing the heartbeat. But, if a particular group of cells in areas remote from the SA node become extra- or hyper-excitable they can take over as the pacemaker for one or several beats, or for a longer term. You might think of the heart's cells as a schoolyard full of young boys playing soccer.

Now there is a diagnostic distinction between myocardial infarction and ischemia—which is usually not possible from clinical or EKG findings alone—has taken on significant therapeutic and economic implications, given the development of new therapies. There may have been EKG with your stress test, and the test showed ST segment elevated with a Q or without a Q wave.

Among many things, appropriate levels help to ensure healthy kidneys and heart, blood sugar levels and the delivery of oxygen to the cells. Improper balances can result in poor circulation, arrythmias, angina, myocardial infarction, sudden cardiac death, dehydration, malnutrition, low blood pressure...... http://www.edreferral.com/consequences_of_ed.

The spread of electricity throughout the heart muscle is possible because all heart muscle cells, not just pacemaker cells, are excitable. Usually, the heart muscle cells keep time more slowly than normal pacemaker cells. This allows the pacemaker cells within the SA node to be in control of generating and pacing the heartbeat.

Dehydration is by far the biggest killer with fever, and fluid loss can be counteracted by monitoring the patient and using IV to push more fluids in. With loss of fluids, cells will start to die, blood pressure will drop and this is not a good situation to be in. From reports I've read with brain cells, they may start to die at 42c. From the patients I've observed in intensive care, they keep the heart rate low, 70-80 to keep it from overworking over long periods of time.

If the heart cells are dead (necrosis) scar tissue will inhibit effective contractions and cardiac output is decreased and functionality impaired. The future probability with stem cell therapy may be a solution.

I am surprised to see your EF is so high when the report indicates hypokinesis (impaired wall movement) and that usually indicates a possiblility the heart cells are not functioning well and existing on a low oxygen level (possible to revive with good blood supply to the area. Akinesis indicates the heart cells are dead. A cath could open a vessel that could feed more oxygenated blood to the area of hypokinesis and that would increase your EF if effective....but you don't have a low EF?

Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.

Many cardiac muscle cells can contract spontaneously, but the cells in the Pacemaker region are, during fetal development, the fastest-beating ones, and the fastest ones normally dominate the whole show. However, many of us have independent-minded cardiac cells that can trigger a contraction (a PVC) if they get the opportunity, and opportunity arises when the Pacemaker's rate slows down--as happens when you're cooling off after exercise, or when you're getting sleepy at bedtime.

Even stunned or hibernating cells will require the oxygen and use it or they will simply shut down and die. As the cells absorb the oxygen, the Thallium is absorbed with it. The scan is not detailed enough to go into single cell detail, but areas will show up where oxygen is absorbed. Dark areas will be dead cells. Areas with a less intensity of colour will depict stunned/hibernating cells because they are not working with the rest of the heart, they are simply surviving in a rest state.

To be consistant, I stated there could be permanent heart damage because everytime there is a deficit of blood going to a specific area of the heart there can be some permanent damage to heart cells that are more vulnerable, and untreated angina can cause permanent damage to some cells and eventually heart failure.

I have been admitted to the hospital on several occasions with chest pain and tachycardia; I was given nitro glycerin patches and ekg's were performed. when i got copies of my records from the hospital there was notations on the ekg's as abnormal.

The sinoatrial node (SA node) is a group of cells positioned on the wall of the right atrium, near the entrance of the superior vena cava. Cells in the SA node will naturally discharge at about 70-80 times per minute. Because the sinoatrial node is responsible for the rest of the heart's electrical activity, it is sometimes called the primary pacemaker, the natural pacemaker.

A heart wall defect indicates there are damaged heart cells that can be caused by a lack of blood/oxygen to the areas provided. Myocardial scar indicates there was a prior heart attack and that caused heart cell necrosis. The conditions will impair heart wall movement (hypokinesis, or akinesis). What this indicates there may be reduced ability of the heart to pump adequately to meet the oxygenated blood demand. Do you have report regarding your heart's ejection fraction (EF)?

By the way...I noticed the ??? near the "natural pacemaker" portion of your post. Thought I'd take a minute to help you understand. The sinus atrial node is a clump of cells in your heart that put out an electrical current that causes the rest of your cells in the atrial center of your heart to contract. The electrical current continues into the ventricular node and causes the bottom of the heart to contract immediately after that.

Pacemaker cells and myocardial cells

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