Decompensated heart failure

Decompensated heart failure is the term used to define heart incapacity of pumping enough blood in the main arteries, according to the organism needs. What distinguishes decompensated heart failure from a compensated heart failure is the fact that defensive mechanisms are not efficient anymore and the blood amount delivered to the tissues is no longer sufficient, which determines a variety of symptoms as we are going to reveal next.
How do you know you have a decompensated heart failure and if u need to go to the hospital? Decompensated heart failure has different manifestations, as following:

•  when the left heart is inefficient, blood will stagnate into the heart chambers forcing them to enlarge or increase the number of muscle fibers in order to increase cardiac force; this is a defensive mechanism, which will compensate for a while the inefficient function of the heart. Once this mechanism is no longer able to control the situation, blood will stagnate in the lungs, increasing the pressure in the pulmonary vessels and from this point on, pulmonary edema (accumulation of water in the lungs) and pulmonary hypertension may occur. All these manifestations are a sign that the heart can no longer compensate its diminished function, so we are facing a decompensated heart failure.
•  in right heart insufficiency, cardiac muscle won’t be able to pump blood into the pulmonary arteries, so the blood will flow back in the venous system, determining accumulation of water in different tissues (lower limbs, abdomen-ascites, pleural space).

In clinical practice, people with decompensated heart failure will experience important shortness of breath, being unable to breathe while lying (a condition known as orthopnoea), blue color of the lips and limbs extremities, fatigue, palpitations or rapid heart beats, incapacity of performing daily activities. In more advanced cases, hypotension, fainting, ischemia of lower limbs, stroke or renal failure may occur, these manifestations being the consequence of the low blood flow in the arteries that feed the brain, kidney, or limbs.

What is the cause for decompensated heart failure?

There are many causes for decompensated heart failure, the most important ones are the following:

•  hypertension-if patients don’t follow the treatment, high blood pressure will increase the labor of an already weak heart, making it impossible to accomplish body needs,
•  salt intake-will favor water accumulation in the body, increasing blood volume and requesting a higher cardiac labor,
• infections: respiratory infections, heart wall infections like myocarditis,
• heart attacks, arrhythmia,
• weight gain is common cause of decompensated heart failure,
• patients that no longer respect their heart medication,
• patients that continue to smoke, drink alcohol, with high levels of blood lipids etc.

What are the steps to follow in decompensated heart failure ? People in this condition must be admitted to hospital, carefully watched, investigated for different conditions that might have provoked decompensated heart failure and follow a well established therapy (diuretics and cardiotonic medication will be needed in order to eliminate the overload of water and increase cardiac muscle force).
People with heart failure will have a different number of hospital admissions, followed by „free” periods of time, when the symptoms will be stable. However, the compliance to medical recommendations will determine how fast this disease will evolve, together with the other conditions we enumerated above. Despite the correct treatment and compliance of the patient, heart failure will progress until the only option left is cardiac transplant, but the speed of this evolution can be controlled by avoiding the conditions that favor heart failure to decompensate.

Please call your doctor to find out mode about decompensated heart failure.

Reperfusion injury

Reperfusion injury has been defined as myocardial tissue blood supply after a period of ischemia. Whether reperfusion merely  accelerates the damage that would have occurred during the initial ischemia  or whether there is a additional injury caused by reperfusion itself is still researched. Although the crucial role of reperfusion injury in revascularization procedures has bees recognized, the etiology and pathogenesis of this phenomenon remain unknown.
Myocardial ischemia accompanied by reperfusion injury followed by complete normalization if it took 5 minutes, by diastolic and systolic dysfunction if ischemia took 15-20 minutes and without return contractile function if ischemia took more than one hour.
The most common cause found in patients who died after reperfusion is hemorrhagic infarction. In myocardial infarction of less than 3 days the cellular response is present throughout the myocardial infarction, in contrast to the distinct zones seen in the non- reperfused myocardial infarctions. Reperfusion itself may produce injury.

The mediators of reperfusion injury

Reperfusion injury

One of the mediators of reperfusion injury is oxygen free radicals. The possible role of reactive oxygen species in reperfusion injury has evolved from our knowledge. They elaborate enzyme systems that rapidly detoxify superoxide and peroxide. The metabolism of reactive oxygen also has damaging effects. The investigators of this event have suspected that even physiological quantities of peroxide may inhibit the aerobic oxidation of pyruvate and thus restrict cellular ATP formation.
Another mediator of reperfusion injury is endothelial dysfunction and microvascular injury. Recent reports indicate that endothelium-dependent relaxation  of coronary microvessels is markedly impaired after ischemia with reperfusion. This microvascular endothelium dysfunction may be caused by blood products or myocardial metabolites that are released during the reperfusion period or by oxygen free radicals.
One of the oldest hypotheses about reperfusion injury involved calcium overload. Other mediators involved in reperfusion injury are altered myocardial metabolism and endogenous protective mechanisms.
There are some cardiovascular risk factors influence reperfusion injury. This are  hypercholesterolemia, very high glucose and hypertension.

Pharmacological methods to attenuate reperfusion injury

There are a number of pharmacological methods for attenuate reperfusion injury. In the treatment of myocardial infarction, restoration of coronary flow as soon as possible is a very important thing to prevent and reduce myocardial necrosis and ischemia. By this treatment ensure a reduction of mortality,  complications and a good prognosis in infarction. Early myocardial reperfusion injury prevent necrosis; in this way systolic and diastolic functions are established and are preventable fatal arrhythmias. In the early hours of  infarction,  reperfusion injury offers the greatest benefits: higher thrombus lysis.
Anti-ischemic therapy and lytic therapy has an important role to reduce myocardial energy demand. There are three revascularizations methods: trombembolitic treatment,  coronary angioplasty and coronary bypass. To thrombolytic treatment add anticoagulant and antithrombotic treatment and GP IIb/IIIa blockers. Thrombolytic agents currently used are streptokinase, tissue plasminogen activator and urokinase.

Conclusion for reperfusion injury

In conclusion the beneficial effect of fast recanalization may be offset by reperfusion injury.

Stents in the heart

Stents in the heart are small medical devices (small mesh tubes) used to treat narrowed arteries (arteries are blood vessels that carry blood from heart to the tissues). The procedure of placing stents in the heart is called angioplasty. Angioplasty alone, without stent placement is associated with a high risk of recurrence of the arterial blockage, in months or years after the procedure. That is why placing stents in the heart solved this disadvantage of the angioplasty, maintaining blood vessels opened and avoiding heart surgery. The risk that the arteries will renarrow is 10-20%  in the first year after angioplasty, while in the absence of a stent the risk is twice as much.

Stents in the heart are usually made of metal mesh or fabric (these ones are used in larger arteries). Some of these stents contain a special substance that prevent blood from coagulating and are called drug-eluting stents.

How are stents in the heart placed? 

Doctors use a balloon inside the artery to compress the plaque (deposits of fats in the arteries wall, also called atherosclerosis) and widen the passage (the arterial lumen through which will flow blood). After this, they place the stent in order to maintain the passage (the artery lumen) opened.

How do we prepare patients before placing stents in the heart?

Patients should be well informed about the stents in the heart procedure, about the risks and the special precautions. These are a few questions u must always ask your doctor about:

•  Why is it performed?
•  How is it performed?
•  What are the risks and precautions of this procedure?
•  Is there any other alternative?
•  What happens if I refuse this procedure?
•  Always sign a consent paper.

Why are stents in the heart placed for?

The purpose for stents in the heart placement is to keep the arterial lumen opened and allow blood to flow, in this way tissues will receive enough blood and the symptoms of ischemia (oxygen deprivation) will be relieved.

• For carotid arteries blockage: fat deposits in carotid arteries wall (also called plaques, they are a manifestation of the disease named atherosclerosis) can determine neurologic symptoms like dizziness, fainting, headache, memory and concentration problems and in severe cases even stroke.
• For coronary vessels (blood vessels that supply blood for heart tissues): a special tube called catheter is introduced in the femoral artery (the main artery of the lower limb) and it is conducted in the arterial system until it reaches the coronary arteries. In that moment, a special substance is pumped into the catheter in order to view the arteries and the blockage. This catheter has a tiny balloon on its tip, which is inflated in the narrowed area, compressing the atheroma (the plaque of fats from the artery wall that blocks blood flow) and enlarging the lumen. After this a stent may be placed to keep the lumen opened.
• For kidney or leg arteries, aneurysm of the aorta.
  

What are the common precautions after placing stents in the heart?

•  blood clotting precautions: in order to prevent blood clotting, patients with stents in the heart have to take antiplatelet medication (aspirin, clopidogrel)
•  if the stent is made of metal, than the patient can’t have MRI (magnetic resonance imaging)
•  avoid vigorous effort early after the stent placement procedure.
  

What risks are related to stents in the heart?

•  restenosis- blood vessel becomes blocked and narrow again, despite the angioplasty procedure
•  about 1 or 2 percent of the patients with a stented artery are at risk of developing a cloth at the stent site; the consequence of this complication can be a heart attack. This complication is more frequent in the first year after stent placement and can be prevented by antiplatelet medication (like aspirin, clopidogrel).
•  bleeding at the site of the catheter insertion into the skin
•  damage of the blood vessel produced by the catheter
•  irregular heart beats
•  infection or allergic reaction (due to the substance used to view the arterial lumen)

Stents in the heart brought a significant contribution in cardiology, saving and improving life in patients with heart attack and coronary disease.