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Chest pain symptoms

Geplaatst: wo mei 18, 2011 7:00 am
door Shinobi
Hello
I just joined this site. I have been hypertensive for a number of years.I started feeling a pain in my chest about November last year(2010).I have been taking Amlodipine(Norvasc) and a diuretic for control of the High blood pressure.I decided to do an ultrasound scan and the result was 1) Congestion of the upper chamber of the heart. 2) Pronounced thickening of the ventricular walls , due to a consistent high output of blood, caused by a weakening of the ventricular muscles, resulting in a partial blockage of key vessels. Also, a heavy congestion of the cardiac cavity was observed. i presently do not get tired, do not eat lots of sugar, and can skip a meal, or even eat 3 hours later. i have also tried to reduce my salt intake

Geplaatst: wo mei 18, 2011 8:34 pm
door Corrij (therapeut)
Hello Shinobi,

Welcome on this forum.

What is your bloodpressure at this moment?

The two upper chambers in your heart are called the atria . The atria are the receiving chambers of your heart. When blood flows into your heart from the body or lungs, it always flows into either the right or left atrium—never anywhere else. (One upper chamber is called an atrium. Both upper chambers together are called the atria.)

The two lower chambers in your heart are called ventricles . The ventricles are the pumping chambers of your heart. When blood leaves your heart, it is always pumped out from the ventricles—never from anywhere else. The ventricles are very strong because they have to pump hard enough to push blood through your lungs and entire body.

A wall, called the septum, separates the left and right sides of your heart. Blood that hasn't yet been to the lungs (blood with no oxygen) stays on the right side of the septum. Blood returning from the lungs (blood with oxygen) stays on the left side of the septum.


Left ventricular hypertrophy is enlargement (hypertrophy) of the muscle tissue that makes up the wall of your heart's main pumping chamber (left ventricle).

Left ventricular hypertrophy develops in response to some factor, such as high blood pressure, that requires the left ventricle to work harder. As the workload increases, the walls of the chamber grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart.

Left ventricular hypertrophy (LVH) is more common in people who have high blood pressure or other heart problems.
Symptoms

Left ventricular hypertrophy usually develops gradually. You may experience no signs or symptoms, especially during the early stages of the condition. As left ventricular hypertrophy progresses and complications develop, you may experience these left ventricular hypertrophy symptoms:
•Shortness of breath
•Chest pain
•Sensation of rapid, fluttering or pounding heartbeats (palpitations)
•Dizziness
•Fainting
•Rapid exhaustion with physical activity

Left ventricular hypertrophy can happen when one or more things make your heart work harder than normal to pump blood to your body. For example, if you have high blood pressure, the muscles of the left ventricle must contract more forcefully than normal in order to counter the effect of the elevated blood pressure.

The work of adapting to high blood pressure may result in larger muscle tissue in the walls of the left ventricle. The increase in muscle mass causes the heart to function poorly.

Factors that can cause your heart to work harder include the following:
•High blood pressure (hypertension). This condition is the most common cause of left ventricular hypertrophy. A blood pressure reading is given in a unit of measure called millimeters of mercury (mm Hg). Hypertension is generally defined as systolic pressure greater than 140 mm Hg and a diastolic pressure greater than 90 mm Hg, or 140/90 mm Hg.(7) Systolic pressure is blood pressure while the heart contracts, and diastolic pressure is blood pressure while the heart rests between beats.

I have some questions for you,

•What are your symptoms?
•When did you first begin experiencing symptoms?
•Have your symptoms gotten worse over time?
•Do your symptoms include chest pain?
•Do your symptoms include rapid, fluttering or pounding heartbeats?
•Do your symptoms include dizziness? Have you ever fainted?
•Have you had difficulty breathing?
•Does exercise or physical exertion make your symptoms worse?
•Does lying down make your symptoms worse?
•Have you ever coughed up blood?
•Are you aware of ever having rheumatic fever?
•Are you aware of any history of heart problems in your family?
•Are you being treated or have you recently been treated for any other health conditions?
•Do you or did you smoke? How much?
•Do you use alcohol or caffeine? How much?

greetings,
Corrij

Chest pain symptoms

Geplaatst: do mei 19, 2011 7:44 am
door Shinobi
I started having symptoms of a pain in the chest November last year(2010).I can also remember feeling faint sometimes, after bending down. It hasnt gotten worse with time.It does not include rapid fluttering heartbeats.

I have not yet experienced difficulty breathing.Exercise does not make it worse.It seems like for now, after some aerobics, the fresh air makes me feel better.Lying down does not make it worse.I have never coughed blood.I have never had rheumatic fever.

My mother had high blood pressure and later on in her years developed a heart problem where her blood pressure started to drop.She later died in her sleep before she could be operated on surgically, after it was diagnosed.I do not smoke and neither do I take alcoholl. I remember I used to take red bull and power horse,which I believe contain caffeine and taurine.I also do take coffee.

Chest pain symptoms

Geplaatst: do mei 19, 2011 1:45 pm
door Shinobi
I forgot to mention to you that my blood pressure as of this morning is 140/93.I also do take Amlodipine 10mg and also Normoretic(Amioride hydrochloride 5g,Hydrochlorothiazide 50g) daily.

Geplaatst: do mei 19, 2011 8:43 pm
door Corrij (therapeut)
Hello Shinobi,

What`s your cardiologist told you about your healthproblems?
Did he used the term cardiomyopathy?

I will suggest the following,

200 mg ubiquinol a day
acetyl carnitine 1500 mg a day

The acetyl carnitine must always be taken on a empty stomach!

L-carnitine is essential for the transport of fatty acids into the heart muscle and mitochondria for energy production and is sensitive to the level of oxygen in the heart muscle. Studies have shown that patients with CHF who take L-carnitine have improved ejection fraction . There is evidence that L-carnitine helps the heart by preventing the enlargement of the left ventricle, which is a critical step in the progression of CHF. Studies have shown that L-carnitine can help prevent left ventricular enlargement after bypass surgery in patients who have had a heart attack . The same results were found among patients who have had an acute heart attack . By improving ejection fraction and preventing enlargement of the left ventricle, L-carnitine addresses two of the most serious problems associated with CHF.

CoQ10 Improves Heart Function
Although CoQ10 is found naturally in all cells, it is particularly concentrated in tissues having high energy requirements, such as the heart. In 1972, researchers documented a link between CoQ10 deficiency and human heart disease. Since that time, scores of articles have been published on the multiple benefits of CoQ10 for heart health. CoQ10 plays a key role in energy production and all energy-dependent processes, especially heart muscle contraction.

A deficiency of CoQ10 has been documented in various types of cardiovascular disease. In addition, CoQ10, as ubiquinol, has been shown to be a potent antioxidant that protects LDL cholesterol from oxidation. This finding has important implications for heart health, because oxidation of LDL is believed to be an initiating factor in the development of atherosclerosis and clogged arteries.

Other research has shown CoQ10 to significantly improve heart function in patients with cardiomyopathy, a weakening of the heart muscle that increases the risk for abrupt cardiac death. It is well known that cardiomyopathy is caused by a decrease in cellular energy production and a disruption in energy flow. Since CoQ10 is documented as being absolutely vital for optimal heart energy and pumping ability, its potential benefit for cardiomyopathy is not surprising.


greetings,
Corrij

Geplaatst: wo aug 10, 2011 6:33 pm
door Shinobi
Hello Corrij. I had an echocardiogram done yesterday. It was discovered that my left ventricle and left atrium were enlarged. The diagnosis was "Eccentric left ventricular Hypertrophy and dilatation. Good global systolic function. No regional wall motion anomaly. Enlarged left atrial size. Normal size right heart. No intracardiac clot or vegetation seen. No pericardial effusion seen. The interatrial and interventricular septae appear intact. Mitral valves Thin and mobile. Aortic valves structurally normal with good mobility. Tricuspid valves Thin and mobile. Diastolic dysfunction present.

I have been using 1000mg of L-Carnitine for a while since you recommended it. I also use L-Arginine 500mg.I am also using Ethylene Diamine tetracetic acid 300mg for chelation and clearing my blood vessels of excess Calcium, and in addition, Norvasc(Amlodipine)10mg and Normoretic( Amiloride Hydrochloride 5mg and Hydroclorothiazide 50mg) to control my High blood pressure. My ejection fraction was 70%

Please, do I need to do anything else. I was told that the enlarged Left Atrium and ventricle were due to a poor control of my High blood pressure.
Thanks

Geplaatst: vr aug 12, 2011 2:53 pm
door Corrij (therapeut)
Hello Shinobi,

You can add,

12 gram Ribose
1500 mg of taurine

CHF occurs when the heart muscle weakens. When this happens, the heart can’t pump a sufficient volume of blood to supply the body’s need for oxygen, a condition also known as ischemia. Hypertension, coronary artery disease and cardiomyopathy are all linked to the development of congestive heart failure and the accompanying systolic and diastolic cardiac dysfunction. With heart failure, many organs are deprived of enough oxygen and nutrients, and damage occurs.

ATP’s Role in Heart Health

Adenosine-5’-triphosphate (ATP) plays an integral role in heart function. ATP shuttles chemical energy within the cells for metabolism and is the main energy source for the majority of cellular functions, including DNA and RNA synthesis. If a person is stressed by poor heart function or over exertion in exercise, they need an increased ATP supply to recover properly.

During the oxygen-deprived state of ischemia, the heart loses as much as 50 percent of its ATP stores. Even after normal blood flow and oxygen levels are restored it can take as much as ten days for ATP levels to rebound enough for the heart to rebuild its cellular energy and normalize cardiac function.

Improving Cardiac Energy

D-Ribose is the exclusive sugar component of ATP and the nucleic acids DNA and RNA. As the building block for ATP, DNA and RNA, D-Ribose can help the heart recover from a low oxygen state.

Under certain abnormal cardiac conditions, nucleotides (particularly ATP, ADP, and AMP) are degraded and lost from the heart. The heart’s ability to resynthesize ATP is then limited by the supply of D-Ribose, which is a necessary component of ATP, ADP and AMP.

After cellular damage, DNA and RNA must be doubled for the cells to divide properly and repair themselves. Without D-Ribose, this repair process could not occur. D-Ribose, therefore, plays a critical role in recovery from injury through its ability to repair DNA and RNA and to increase ATP levels. However, the body’s rate of D-Ribose production is constant. It doesn’t accelerate according to need, which can have disastrous consequences for recovery efforts, especially during congestive heart failure and ischemic heart disease.

Researcher Heinz-Gerd Zimmer at the University of Munich pioneered much of the early work that made the connection between D-Ribose and heart function. Since the 1970s, Zimmer has conducted many animal studies that confirm D-Ribose’s cardiovascular effects. In rodents with depressed heart function and reduced ATP levels, D-Ribose, when continuously infused for 24 hours, prevented the ATP reduction that occurred in untreated animals, and normalized left ventricular function.

Another of Zimmer’s studies explored D-Ribose’s effect in the heart muscle of rats after a low-oxygen (hypoxic) state was induced. Even after a brief period of ischemia, the heart is very slow at replenishing its ATP pool. Zimmer and his colleagues proved that continuous i.v. infusion of D-Ribose during recovery from 15 minutes of myocardial ischemia in rats leads to restoration of the cardiac ATP pool within 12 hours, whereas 72 hours are needed for ATP normalization without any intervention.

In an animal model of heart transplantation, Zimmer and colleagues also found that D-Ribose treatment maintains ATP at a higher level in preserved rat hearts and that D-Ribose may be able to prolong the preservation time of donor hearts.

John Foker, another researcher who recognized D-Ribose’s importance in heart health, produced myocardial ischemia in dogs, then, during the recovery phase, administered by infusion either D-Ribose or saline. In both the D-Ribose and saline groups, myocardial ATP levels fell by at least 50 percent at the end of ischemia. No significant ATP recovery occurred after 24 hours in the control dogs, but in the D-Ribose-treated animals, ATP levels rebounded by 85 percent by 24 hours.

In a similar experiment, Foker found that it took 9.9 days for ATP levels to fully recover after ischemia in untreated dogs, but only 1.2 days to recover in dogs given a D-Ribose infusion.

Recently, in a prospective, double blind, randomized, crossover design study, scientists assessed oral D-Ribose supplementation on cardiac function and quality of life in 15 patients with chronic coronary artery disease and congestive heart failure. The study consisted of two treatment periods of 3 weeks, during which either oral D-Ribose or placebo was administered. A 1-week wash out period followed, and then subjects who had been taking the placebo began taking the D-Ribose and subjects who had taken the D-Ribose took the placebo. The administration of D-Ribose enhanced left ventricular function and other markers of heart function. D-Ribose also resulted in a significant improvement of the patients’ quality of life. The placebo did not result in any improvements.

In the cell, taurine keeps potassium and magnesium inside the cell while keeping excessive sodium out. In this sense it works like a diuretic. But unlike prescription diuretics, it is not a cellular poison. It does not act against the kidney, but improves kidney function instead. Taurine is very useful in fighting tissue swelling and fluid accumulation. People with heart failure, liver disease , late stage ovarian cancer, congestive heart failure frequently have unwanted fluid accumulation inside their bodies and people who take long plan flight usually have slight fluid retention.

Taurine has been very successfully used to treat people with high blood pressure. When excessive fluid is normalized, blood pressure becomes normalized. Taurine functions to dampen the sympathetic nervous system, thereby relieving arterial spasm. When blood vessels relax, the body’s blood pressure will fall.

There have been studies showing the positive effectiveness of taurine on heart failure. Aside from having diuretic properties, taurine is able to strengthen the heart muscles and maintain proper calcium balance. Together with Coq10 and
carnitine, taurine is able to regulate the heart’s contractility and guard against toxic threat of chemotherapeutic drugs such as adriamycin(doxorubicin). .

Working together with magnesium, taurine also is able to regulate heart rhythm and help to stabilize it.

Taurine also on a empty stomach!

greetings,
Corrij