what is acute coronary syndrome?

Question

my father died because of this deases. and i didnt understand about this. before he didnt have any chest pain. how it will possible to him to die because of it

Answer 1

An acute coronary syndrome (ACS) is a set of signs and symptoms, usually (but not always) a combination of chest pain and other features, interpreted as being the result of abruptly decreased blood flow to the heart (cardiac ischemia); the most common cause for this is the disruption of atherosclerotic plaque in an epicardial coronary artery. The subtypes of acute coronary syndrome include unstable angina (UA, not associated with heart muscle damage), and two forms of myocardial infarction (heart attack), in which heart muscle is damaged.

Basically, the bloodflow to the heart was decreased, the heart tissue starved and died, and the heart stopped beating as a result. No heart beat leads to immediate death.

Answer 2

Firstly, I am terribly sorry for your loss. It must be difficult to lose someone so quickly and without warning.

ACS encompasses 3 entities.
1. Non ST elevation Myocardial Ischaemia.
2. ST Elevation Myocardial Ischaemia.
3. Unstable angina

The first 2 are called "heart attacks".

What does it all mean? In simple terms, it just means that the heart muscle is starved of oxygen to the extent that there is heart muscle cell (myocardium) death. The heart is dying without oxygen. The "ST elevation" in the terms refer to the changes in the electrical tracing of the hear (ECG). Not very relevant to a layperson.

Why divide it into 3 entities? Because the management for each is different (it's for us doctors to follow an algorithm of management, as well as to see which patients have a better outcomes etc.)

Many people have very minimal symptoms of ACS, especially if they are diabetic, women or old.

ACS also manifests as sudden death (means exactly as it sounds), as in a person can be perfectly fine one moment, and then without warning, collapse. The main cause for this sudden collapse is that the heart muscle, being starved for oxygen, start being very sensitive and finicky, and beat at a very irregular fast rhythm called Ventricular Tachycardia OR Ventricular Fibrillation. When this abnormal rhythm occurs, the heart does not pump out blood as well as it should, and it leads to there not being enough oxygen sent to important organs like the brain/heart/etc. It takes only 1-2 minutes before the person is unconcious and 4 minutes before the brain gets starved for oxygen, 30 minutes for the heart muscle to start dying and so forth.

As you see, the timeline is extremely short. This would explain why he did not have any chest pain prior.

I hope that it clears things up somewhat for you.

Answer 3

It's sweet that you're concerned about your mom. Heart issues that manifest while exercising (vs. those that cannot be induced via exercise) are serious. She should see her doc and explain what happened, and perhaps be seen by a cardiologist just to see her/your mind at ease. If it's a heart issue, there are a zillion treatments. Better safe than sorry.

Answer 4

I'm sorry to hear that about your father.
I do know people with ACS, die because of SADS, sudden arterial death syndrome.

You can find more information on wikipedia, but the previous poster explains very well.

Answer 5

I am sorry to read about your father, my heartfelt condolences, this article I have searched out for you:

Background: The initial diagnosis of acute coronary syndrome (ACS) is based entirely on history, risk factors, and, to a lesser extent, ECG findings. The symptoms are due to myocardial ischemia, the underlying cause of which is an imbalance between supply and demand of myocardial oxygen.

Patients with ACS include those whose clinical presentations cover the following range of diagnoses: unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). This ACS spectrum concept is a useful framework for developing therapeutic strategies.

Pathophysiology: Myocardial ischemia is most often due to atherosclerotic plaques, which reduce the blood supply to a portion of myocardium. Initially, the plaques allow sufficient blood flow to match myocardial demand. When myocardial demand increases, the areas of narrowing may become clinically significant and precipitate angina. Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest, and without recent change in frequency or severity of activity that produce symptoms, is called chronic stable angina. Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombus forms. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina.

Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery. Angiographic evidence of coronary thrombus formation may be seen in more than 90% of patients with STEMI but in only 1% of patients with stable angina and about 35-75% of patients with unstable angina or NSTEMI. However, not every STEMI evolves into a Q-wave MI; likewise, a patient with NSTEMI may develop Q waves.

The excessive mortality rate of coronary heart disease is primarily due to rupture and thrombosis of the atherosclerotic plaque. Inflammation plays a critical role in plaque destabilization and is widespread in the coronary and remote vascular beds. Systemic inflammatory, thrombotic, and hemodynamic factors are relevant to the outcome. Evidence indicates that platelets contribute to promoting plaque inflammation as well as thrombosis. A new theory of unbalanced cytokine-mediated inflammation is emerging, providing an opportunity for intervention.

A less common cause of angina is dynamic obstruction, which may be caused by intense focal spasm of a segment of an epicardial artery (Prinzmetal angina). Coronary vasospasm is a frequent complication in patients with connective tissue disease. Other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, such as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina as a baseline medical condition.

Spontaneous and cocaine-related coronary artery dissection remains an unusual cause of ACS and should be included in the differential diagnosis, especially when a younger female or cocaine user is being evaluated. An early clinical suspicion of this disease is necessary for a good outcome. Cardiology consultation should be obtained for consideration for urgent percutaneous coronary intervention.

Although rare, pediatric and adult ACS may result from the following (see Myocardial Infarction in Childhood):

* ACS may occur with Marfan syndrome; Kawasaki disease; Takayasu arteritis; or cystic medial necrosis with aortic root dilatation, aneurysm formation, and dissection into the coronary artery.

* Anomalous origin of the left coronary artery from the pulmonary artery may occur as unexplained sudden death in a neonate.

* Coronary artery ostial stenosis may occur after repair of a transposition of the great arteries in the neonatal period.

* An aberrant left main coronary artery with its origin at the right sinus of Valsalva may cause ACS, especially with exertion.

* Traumatic myocardial infarction can occur in patients at any age.

* Accelerated atherosclerosis is known to occur in cardiac transplant recipients on immunosuppressive therapy.

* Progeria

Irrespective of the cause of unstable angina, the result of persistent ischemia is myocardial infarction (MI).

Frequency:

* In the US: Although the exact incidence of ACS is difficult to ascertain, hospital discharge data indicate that 1,680,000 unique discharges for ACS occurred in 2001.

* Internationally: In Britain, annual incidence of angina is estimated at 1.1 cases per 1000 males and 0.5 cases per 1000 females aged 31-70 years. In Sweden, chest pain of ischemic origin is thought to affect 5% of all males aged 50-57 years. In industrialized countries, annual incidence of unstable angina is approximately 6 cases per 10,000 people.

Mortality/Morbidity: When the only treatment for angina was nitroglycerin and limitation of activity, patients with newly diagnosed angina had a 40% incidence of MI and a 17% mortality rate within 3 months. A recent study shows that the 30-day mortality from ACS has decreased as treatment has improved, a statistically significant 47% relative decrease in 30-day mortality among newly diagnosed ACS from 1987-2000. This decrease in mortality is attributed to aspirin, glycoprotein (GP) IIb/IIIa blockers, and coronary revascularization via medical intervention or procedures.

Clinical characteristics associated with a poor prognosis include advanced age, male sex, prior MI, diabetes, hypertension, and multiple-vessel or left-mainstem disease.

Sex: Incidence is higher in males among all patients younger than 70 years. This is due to the cardioprotective effect of estrogen in females. At 15 years postmenopause, the incidence of angina occurs with equal frequency in both sexes. Evidence exists that women more often have coronary events without typical symptoms, which might explain the frequent failure to initially diagnose ACS in women.

Age: ACS becomes progressively more common with increasing age. In persons aged 40-70 years, ACS is diagnosed more often in men than in women. In persons older than 70 years, men and women are affected equally.

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History:

* Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It usually is described as a sensation of chest pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand.

* Not all patients experience chest pain. Some present with only neck, jaw, ear, arm, or epigastric discomfort.

* Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalents.

* A patient may present to the ED because of a change in pattern or severity of symptoms. A new case of angina is more difficult to diagnose because symptoms are often vague and similar to those caused by other conditions (eg, indigestion, anxiety).

* Patients may have no pain and may only complain of episodic shortness of breath, weakness, lightheadedness, diaphoresis, or nausea and vomiting.

* Patients may complain of the following:

o Palpitations

o Pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to neck, shoulder, jaw, back, upper abdomen, or either arm

o Exertional dyspnea that resolves with pain or rest

o Diaphoresis from sympathetic discharge

o Nausea from vagal stimulation

o Decreased exercise tolerance

o Patients with diabetes and elderly patients are more likely to have atypical presentations and offer only vague complaints, such as weakness, dyspnea, lightheadedness, and nausea.

For further details go the link given below.

http://www.emedicine.com/EMERG/topic31.htm