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Can a surgical implant in the heart prevent blood clot formation during atrial fibrillation?

Teachable moment in classrooms:

  1. heart chapter – description of blood flow through the chambers of the  heart 
  2. blood chapter – mechanism of blood clotting
  3. hemodynamics chapter – connection of atria to systemic veins and systemic arteries

The news item:  Recently the following report appeared online:

Durham VA Performs Second Watchman Procedure in North Carolina, First in VISN 6 | VA Durham health care | Veterans Affairs

On August 21, 2023, the Durham VA Health Care System achieved a significant medical milestone as it became the second hospital in North Carolina and the first facility in VA’s Mid-Atlantic Health Care Network to perform the Watchman FLX Left Atrial Appendage Closure Device procedure.

The article describes the first implantation of the Watchman FLX Pro device for left atrial appendage closure, and that the device is used to reduce the incidence of stroke in patients with atrial fibrillation who can not tolerate long-term use of blood thinners. The article also describes atrial fibrillation as a form of arrhythmia.

So, Why Do I Care??  There are over 10 million Americans with atrial fibrillation, and all of them have an increased risk of stroke. Because strokes can have debilitating consequences, it is important to prevent atrial fibrillation or stop the process of blood clot formation. While pacemakers and blood thinners serve to prevent atrial fibrillation in most people, in patients who cannot tolerate long-term blood thinner treatment other treatment alternatives must be used.

Plain English, Please!!!  First, let’s talk about the connection between stroke and the atria of the heart. A stroke is a consequence of a blood clot blocking blood flow through an artery in the brain. During atrial fibrillation the muscle of the atria shivers, and the ejection of blood from the atria slows down. Think about when your teeth chatter in the cold. Your jaw muscles shiver and cannot create force. Similarly, the atria cannot create force to push out blood. Blood clots form with ease in such very slowly flowing blood. The critical location for the formation of blood clots can be pinpointed to the appendage of the left atrium. From there normal blood flow takes the blood clots from the left atrium to the arteries of the brain.

Second, let’s talk about the atrial appendage. While the atrium is a chamber shaped like a wide-open cave, the appendage is shaped like a pocket of a pita bread. The opening of the pocket is connected to the

How can finerenone help patients with both kidney disease and heart disease?

Teachable moment in classrooms:

  1. urinary system chapter – parts of the nephron and their functions
  2. endocrine system chapter – location and action of receptors for lipid-soluble hormones
  3. heart chapter within cardiovascular system – location of myocardium in the heart wall

The news item:  Recently the following article appeared online:

Utilization of Finerenone by Patients With T2D, CKD | Docwire News

Two years after its approval, researchers studied the use of finerenone in adults with type 2 diabetes and chronic kidney disease (CKD).

The report states that finerenone – a mineralocorticoid receptor antagonist – is approved for several medical conditions (type 2 diabetes, chronic kidney disease, end-stage renal disease, heart failure) where glomerular filtration rate was declining. The author states that utilization rate is still low for this drug.

So, Why Do I Care??  In the USA alone the combined number of people suffering from type II diabetes, chronic kidney disorder (CKD), end-stage renal disease (ESRD) and heart failure is over 100 million. Those disorders cause the death of over 500,000 people every year, and force many patients into hospitalizations, and into major changes in the quality of life. Therefore, it is worth finding and using new pharmaceutical treatments that may lower those disease and death numbers.

Plain English, Please!!! First, let’s talk about what is the shared, common, physiological malfunction in CKD, ESRD, and heart failure. In all three disorders damaged cells start inflammation, and the tissue is repaired by formation of scar tissue. In the case of CKD and ESRD the kidney accumulates unusually large amount of connective tissue (develops fibrosis) made by overstimulated fibroblast. In heart failure the myocardium portion of the heart wall accumulates unusually large amount of connective tissue. In the kidneys the filtration by the nephrons is slowed down by fibrosis, while in the heart the contraction of the ventricles is made difficult by the fibrosis.

Second, let’s talk about why fibrosis appears in the kidneys and in the heart. During early stage kidney disease and early-stage heart disease the cells of the nephron in the kidneys, and the cardiac muscle cells

Can we lower the need for hospitalization by preventing the clumping of proteins in the heart?

Teachable moment in classrooms:

  1. cellular basis of life chapter – concept of one gene, one protein
  2. cellular basis of life chapter – concept of gene mutation leading to protein malfunction
  3. heart chapter – layers of the heart wall
  4. heart chapter – conduction system of the heart and arrhythmias

The news item:  Recently the following article appeared online:

NHS England ” First ever life-saving treatment for rare heart condition available on the NHS

NHS patients with a life-threatening heart condition are set to benefit from a cutting-edge new medicine which can significantly reduce the risk of hospitalisation and death. The drug, tafamidis, is the first ever approved treatment for a cohort of patients in England with a rare heart condition known as transthyretin amyloidosis cardiomyopathy (ATTR-CM), where clumps […]

The reporting states that the drug tafamidis treats patients with transthyretin amyloidosis cardiomyopathy (ATTR-CM), and that this disease comes from deposition of clumped proteins in the heart, presents symptoms of shortness of breath, fatigue, fainting, and may result in heart failure and death. In clinical trials tafamidis reduced hospitalizations by 41%.

So, Why Do I Care??  ATTR-CM currently affects about 6 million people un the USA, and 5-7000 new diagnoses happen each year. Heart disease limits daily activity of the patients, and lower their quality of life; therefore, designing treatments is always a positive development.  Because amyloidosis can appear in many organs, tafamidis might show the potential path to the treatment of those disorders.

Plain English, Please!!!  First, let’s talk about what amyloidosis is. In general terms, amyloidosis is an abnormal accumulation of proteins into clumps large enough to be seen through a light microscope. Many times those clumps interfere with the normal functioning of organs. In the case of ATTR-CM the transthyretin gene has mutations that cause the transthyretin protein to be misshaped. The normal transthyretin proteins join together in groups of four, because some amino acids create sticky surfaces that hold the four proteins together. Picture four eggs, each having a drop of glue at the pointed end. When four eggs are touching each other at their pointed ends they are stuck together like the four transthyretin proteins, and because the sticky surfaces are all covered up, no more eggs can be part of this complex.  When the transthyretin protein is misshapen, the positions of the sticky surfaces change on the protein, and thousands of eggs (proteins) would stick to each other randomly, forming large clumps of eggs (proteins), the amyloids.

Second, let’s talk about how amyloidosis damages the heart. The clumps of transthyretin pile up in between the cardiac muscle cells, and with time connective tissue builds up next to the amyloids. The

Can you die by drinking too much stimulants like charged lemonade?

Teachable moment in classrooms:

  1. heart chapter – order of contraction of chambers during cardiac cycle
  2. heart chapter – contraction of cardiac muscle cells are causing the contraction of heart chambers
  3. heart chapter – structures in the conduction system of the heart
  4. heart chapter – relationship of the ECG wave forms to contraction of heart chambers

The news item: Recently the following news appeared online:

Family sues Panera Bread after college student who drank Charged Lemonade dies

Panera Bread is facing a lawsuit from the family of 21-year-old University of Pennsylvania student Sarah Katz, who died after drinking a “charged lemonade.”

The article states that a college student age 21 died of cardiac arrest as a consequence of drinking a “Charged lemonade” drink.The drink had 390 mg of caffeine. The article also states that the student has been suffering from long QT syndrome which is caused by a malfunctioning of the heart’s electrical system.  The syndrome causes fainting or heart palpitations upon excitement or exercise.

So, Why Do I Care??  Disorders of the heart may not show any symptoms during a sedentary life style. In the US alone there are over 100,000 people who has the long QT syndrome, and 2000-3000 people die a sudden death because of it. Because the symptoms appear mostly during stressful conditions, and therefore remain hidden in many people. If you know you have a heart disorder it is important to use your prescribed medications, and if you have symptoms of heart disorders then it is important to have them evaluated by medical professionals.

Plain English, Please!!!

First, let’s talk about heart rhythms. In order for the heart to move, to pump blood, the chamber must contract in a sequence during a single heartbeat.  The atria contract first, and then, after a short delay, the ventricles contract. This proper order of contractions is orchestrated by electric impulses from the heart’s natural internal pacemaker, the conduction system. This conduction system activates the muscle of atria or ventricles just like a band-leader of a marching band directs the use of musical instruments during a parade.

Second, let’s talk about long QT syndrome. The name of the syndrome comes from name of wave forms on electrocardiograms. The Q wave represents the first step in the contraction of the ventricles, and the

Can we really grow blood in a laboratory?

Teachable moment in classrooms:

  1. cellular basis of life chapter – concept of one gene, one protein
  2. cellular basis of life chapter – concept of gene mutation leading to protein malfunction
  3. cardiovascular system chapter – formation of red blood cells by stem cells in red bone marrow
  4. respiratory system chapter – oxygen transport by hemoglobin in red blood cells

The news item:  Recently the following report appeared online:

Lab-grown blood given to people in world-first clinical trial

It is hoped the blood could revolutionise care for people who need regular donations.

The report described the need for blood transfusion for repeated infusions such as those for sickle cell anemia patients, and the shortage of minor blood types for transfusion. The report briefly described the lifespan of the red blood cells, and the process of growing blood in the lab.

So, Why Do I Care??  Blood transfusion, the administering of blood or red blood cells into the vein of the recipient, is a life saver when the recipient lost lot of blood, or when the red blood cells of the recipient are being damaged because of a disease. As the transfused blood is derived from blood donors who are not always available to donate, the volume of donated blood can be so low as to create a blood shortage.  It would be a great improvement if red blood cells could be “manufactured” on demand.  That would make blood shortages obsolete. In the US 100,000 people suffer from sickle cell anemia.

Plain English, Please!!!  First, let’s talk about why blood transfusion is a lifesaver clinical intervention, in general. We need red blood cells to transport oxygen from the lungs to all organs of our body. When blood loss or damage to red blood cells (like in sickle cell anemia) decrease the number of oxygen transporter cells, the organs do not receive enough oxygen for normal functioning. It’s like a fleet of trucks delivering bread to a store. If the trucks break down, the bread never get’s to the stores, and the functioning of the store will suffer. In this case the red blood cell trucks deliver oxygen to organs of the body. The most noticeable effect of oxygen deficit is on the skeletal muscles (loss of muscle strength) and on the nervous system (fatigue, tiredness). Restoring the number of red blood cells to normal helps to return the functioning of the body to normal. This why most transfusions do not transfuse whole blood, but only red blood cells.

Second, let’s talk about why sickle cell anemia patients need frequent blood transfusions. In sickle cell anemia patients the mutation of the globin protein of hemoglobin causes the red blood cells to change

Why the test to predict preeclampsia is hailed as a great news?

Teachable moment in classrooms:

  1. blood vessel chapter – layers of the wall of arteries
  2. blood vessel chapter — blood pressure regulation through vasoconstriction and vasodilation
  3. urinary system chapter – filtering membrane of the glomerulus in the renal corpuscle
  4. development chapter – blood vessels in the placenta

The news item:  Recently the following news item appeared online:

FDA approves groundbreaking blood test for early preeclampsia detection in pregnant women

The FDA has approved a new blood test that can detect whether a mother will potentially get preeclampsia within 30 minutes.

The report describes preeclampsia as high blood pressure in pregnant women, and that in the state of Georgia hypertensive disorders are the leading cause of maternal death. The article describes the name of the test: BRAHMS sFlt1/PlGF KRYPTOR.

So, Why Do I Care??  The death of pregnant mothers is a tragic event that could cause the death of their unborn child as well.  When pregnancy-related high blood pressure appears, the medical response depends on how high the blood pressure is. Once a test predicts that preeclampsia will appear in a pregnant woman, the obstetrician can make preparations for monitoring and further possible actions. When the medical professionals are ready to make treatment choices, it is more  likely that the intervention will be successful, and both mother and baby will survive.

Plain English, Please!!!  First, let’s talk about why high blood pressure appears in pregnant women who had normal blood pressure before the pregnancy. By the end of the first month of pregnancy the fetus builds a placenta, an organ that incorporates a layer of the mother’s uterus as well. The purpose of the placenta to provide a place for exchange of oxygen and nutrients from the blood of the mother to the blood of the fetus, and for the exchange of carbon dioxide and other waste products from the blood of the fetus to the blood of the mother. This can be achieved only if a large number of fetal blood vessels and maternal blood vessels are part of the placenta. In the fetuses where the number of blood vessels is low in the placenta, the fetus will be deficient in oxygen, and the blood vessels release stress factors such as placenta growth factor (PlGF), and soluble fms-like tyrosine kinase-1 (sFlt1). Those stress factors reprogram the blood vessels of the mother to contract, and the contracting blood vessels increase blood pressure. Imagine a balloon filled with water. If you squeeze the balloon the force will increase water pressure to the point that balloon may burst. Smooth muscle cells in the wall of arteries do the squeezing (vasoconstriction) that increases blood pressure.

Second, let’s talk about why is preeclampsia harmful. High blood pressure in the mother can cause strokes by dislodging clots from large blood vessels and moving them to the brain where the clots block

How can the genetic engineering treatment of red bone marrow by Zynteglo help beta-thalassemia patients?

Teachable moment in classrooms:

  1. cellular basis of life chapter – concept of one gene, one protein
  2. cellular basis of life chapter – concept of gene mutation leading to protein malfunction
  3. cellular basis of life chapter – mRNA translation is needed for protein synthesis
  4. blood chapter – red blood cells are made in the red bone marrow
  5. blood chapter – the role of globin chains in hemoglobin function

The news item:  Recently the following report appeared:

https://timesnewscity.com/bluebirds-2-8m-gene-therapy-becomes-most-expensive-drug-after-us-approval/

The article states that about 1,500 patients need blood transfusion every 2-5 weeks, and that Zynteglo is a gene therapy.

So, Why Do I Care??

The most severe type of beta-thalassemia causes serious anemia with the symptoms of continuous lethargy, fatigue, tiredness. To fight this, the patients require regular blood transfusions. Those patients expected to live until about the age of 50. in the US there are about 1500-3000 such patients. New treatment approaches give the hope of longer life to those patients.

Plain English, Please!!! First, let’s talk about what beta-thalassemia is. This disorder is caused by the missing beta-globin protein in hemoglobin. The protein is missing because the beta-globin gene has mutations that prevent the mRNA formation for beta-globin. The outcome is that hemoglobin is abnormal, because it is formed only from the alpha-globin proteins. Such abnormal hemoglobin makes cells of the red bone marrow to burst, reducing the production of oxygen transporter red blood cells. The decreased oxygen transport cause anemia, the starvation of cells for oxygen.

Second, let’s talk about how red blood cells are made. The damage of the beta-thalassemia is done in the red bone marrow, where red blood cells are formed. In the red bone marrow the red blood cells move

How can a pharmaceutical such as Entresto treat heart failure?

Teachable moment in classrooms:

  1. heart chapter – functional difference in the thickness of myocardium of atria and ventricle wall
  2. heart chapter – conduction system delivers nerve impulses to myocardium
  3. heart chapter — importance of stroke volume
  4. hemodynamics chapter – effects of angiotensin and ANP on blood pressure and volume

The news item:  Recently the following news report appeared:

Advancement in heart failure medication helping patients at MercyOne

There are some medical issues that are an easy fix and then there are some that are more complex, like heart failure. For those with early signs of heart failure, an advancement in medication is making all the difference for patients at MercyOne…

The article discusses the new drug Entresto that moderates symptoms in heart failure patients. The patient interviewed for this article had Guillain-Barre syndrome that caused severe heart arrhythmia.

So, Why Do I Care??  Heart failure indicates a malfunctioning of one of the most important organ in the body. Over 6 million people in the USA have heart failure, and it is listed as cause of 13% of all deaths.  Heart failure results in worsening quality of life because of the inability to hold a job, inability to participate in social activities and in family life.

Plain English, Please!!! First let’s talk about what heart failure is. Most important to understand here is that heart failure doesn’t mean that the heart stops working. Heart failure means that the heart can not pump enough blood to maintain normal functions of all organs. Heart failure may start with moderately decreased  ability and it may then progress to further loss of pumping to the point where life can not be maintained with very low level of pumping. Loss of pumping ability, the heart failure, may be the consequence of malfunctioning heart valves, arrhythmias (abnormal delivery of nerve impulses to the heart muscle), or the damage or thickening (hypertrophy) of the heart wall.

Second, let’s talk about why hypertrophy of the heart wall can lead to heart failure. While it is intuitive to picture why malfunctioning heart valves, or arrhythmias can cause heart failure, it is not that intuitive to see why thickening (hypertrophy) of the heart wall can be damaging. In most cases hypertrophy thickens

Why are we trying to transplant pig hearts into human beings?

TeachableMedicalNews article 10222022

Teachable moment in classrooms:

  1. chemical basis of life chapter – genetic engineering can remove genes from, or add genes to DNA molecules (the chromosomes)
  2. cellular basis of life chapter – removing a gene removes a protein, while adding a gene adds proteins to the functional toolkit of cells
  3. hear chapter – blood pumping action of left ventricle delivers oxygen, nutrients to all organs
  4. immune system chapter – role of HLA proteins in the recognition of self and non-self antigens

The news item:  Recently the following news article was published:

Two pig heart transplants succeed in brain-dead recipients

Surgeons at New York University (NYU) have successfully transplanted genetically-engineered pig hearts into two brain-dead people, researchers said on Tuesday, moving a step closer to a long-term goal of using pig parts to address the shortage of human organs for transplant.

The article states that experimental transplantation of pig hearts into brain dead humans was carried out, and the hearts remained functional for the three days of the study.  The article also states that the transplanted hearts came from genetically engineered pigs in which 4 genetic alterations were done to prevent rejection, and 6 genetic modifications were done to prevent incompatibilities between pigs and humans.

So, Why Do I Care??  There are about 600,000 people in the US whose heart is about to give out (end stage heart disease), but there are only about 3800 heart transplant operations. Several people die each day because suitable donor hearts are not available for transplantation. If we could routinely transplant pig hearts into humans that would save thousands of lives.

Plain English, Please!!!  First, let’s talk about why people need a heart transplant. End stage heart disease happens either because of the degeneration of heart muscle from coronary artery disease or from viral infection, or because of heart valve problems.  Once the pumping efficiency of the heart drops

How does drug injection into the eye save people from blindness?

TeachableMedicalNews article 05252022

Teachable moment in classrooms:

  1. special senses chapter – location of macula lutea in the retina of the eye
  2. special senses chapter – the photoreceptors rods and cones are in the retina
  3. hemodynamics chapter – capillaries are the thinnest blood vessels
  4. hemodynamics chapter – endothelial cell location in capillaries

The news item:  Recently a report appeared about a drug that restores eyesight:

New technology helps Georgetown veteran restore his eyesight

If you’re living with blurry vision, there’s a chance a new device can help you get your eyesight back without frequent visits to the doctor. The newly FDA-approved Susvimo implant helped one Georgetown veteran preserve his vision after being diagnosed with wet age-related macular degeneration.

The article states that AMD (wet, age-related macular degeneration) is the leading cause of blindness over the age 60, that this disorder is caused by growth and scarring of blood vessels under the retina, and that the drug-delivery implant has restored vision in 90% of the treated individuals.

So, Why Do I Care??  Blindness is a condition where a significant part of the eyesight is lost, and such loss has a severe negative impact on people’s lives. In the USA alone there are about a million patients with wet age-related macular degeneration, and without treatment most of them will go blind.

Plain English, Please!!!   First, let’s talk about how the structure called macula plays a role in our vision. When we say we see something, the image of that something has to be turned into a nerve impulse so

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