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Showing posts with label angina. Show all posts
Showing posts with label angina. Show all posts

What is Unstable Angina?

The following three patient groups may be said to have unstable angina pectoris.
  • Patients with new onset (< 2 months) angina that is severe and/or frequent (>) 3 episodes/day
  • Patients with accelerating angina, that is, those with chronic stable angina who develop angina that is distinctly more frequent, severe, prolonged or precipitated by less exertion than previously.
  • Those with angina at rest.
  • When unstable angina is accompanied by objective ECG evidence of transient myocardial ischaemia, this is associated with critical stenosis in one or more epicardial coronary arteries in about 85%.

What are the causes of chest pain?

Chest pain is the  most important symptom in cardiovascular diseases.
It can be due to

  • Cardiovascular origin
  • Non-cardiovascular origin
  • Cardiovascular causes of chest pain 
  • Anginal pain, usually not < 1min, not > 20 min
  • Pericardial pain
  • Aortic pain.

Non-cardiovascular origin

  • Chest wall pain
  • Respiratory system - pleura, upper airway
  • Mediastinum - oesophagus and other tissues
  • Psychogenic.

What are the causes of Angina Pectoris?

Angina can be caused by abnormal coronaries or normal coronaries
Angina due to abnormal coronaries
Coronary disease - Atherosclerotic and non - atherosclerotic-Vasculitis, vasospasm, embolism. Congenital anomaly
Angina with normal coronaries
  • Aortic stenosis, HOCM, MVP
  • Hyperviscosity - polycythemia
  • Right ventricular angina seen in pulmonary artery hypertension PAH
  • Systemic hypertension and LVH
  • Severe anemia.
Aortic stenosis: It results in  decreased stroke volume, reducing coronary perfusion and compression of coronaries by hypertrophied myocardium, so decreased oxygen supply and increased oxygen demand by the hypertrophied myocardium. The ischaemic burden is increased by reduced capillary density  and coexistent atherosclerosis.
Aortic regurgitation:Aortic regurgitation results in decreased coronary perfusion as a result of rim off of blood back into the leftventricle  and periphery during diastole; in syphilitic AR, there is coronary ostial stenosis also.
Hypertrophic obstructive cardiomyopathy: mechanism of angina is same as in aortic stenosis.
Systemic hypertension:Systemic hypertension result in  decreased diastolic coronary perfusion as a result of left ventricular hypertrophy.
Severe anaemia
Connective tissue disorders (due to arteritis) 
Extreme tachyarrhythmias.

What are anginal equivalent ?

Anginal equivalents are symptoms of myocardial ischaemia other than angina such as
  • Dyspnoea
  • Faintness
  • Fatigue 
  • Eructations. 
These symptoms are  precipitated by exertion and relieved by rest and nitrates.

Metabolic anti anginals

Following are metabolic antianginal agents

Glucose insulin potassium (GIK) infusion

Reduces the rate of FFA oxidation, with a concomitant increase in glucose oxidation rates by inhibiting enzyme LC 3-KAT(long chain 3 keto acyl coenzyme A thiolase), which is a crucial enzyme in beta oxidation pathway.

Similar to trimetazidine. Acts as a partial fatty acid oxidation inhibitor (only during myocardial ischemia)& stimulates glucose oxidation

It acts by shifting myocardial substrate utilization from fatty acids to carbohydrates through inhibition of CPT 1

Protects cardiac cells against oxidative stress, hypoxia & ischemia. It decreases toxic coenzyme A derivatives.


Pathophysiology of unstable angina

1.Plaque rupture or erosion with superimposed nonocclusive thrombus,is believed to be the most common cause 
2. Dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina] 
3. Progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)] 
4.Secondary UA related to increased myocardial oxygen demand and/or decreased supply (e.g., anemia). 
More than one of these processes may be involved in many patients.

Angina classification

Braunwald’s classification of angina
Class I  - New onset of severe angina or accelerated angina; no rest pain
Class II - Angina at rest within past month but not within preceding 48 hr (angina at rest, subacute)
Class III- Angina at rest within 48 hr (angina at rest, subacute)

Classification based on clinical circumstances
A (secondary angina) - Develops in the presence of extracardiac condition that intensifies myocardial ischemia
B (primary angina) - Develops in the absence of extracardiac condition
C (postinfarction angina) - Develops within 2 weeks after acute myocardial infarction

Classification based on intensity of treatment
(1) - In the absence of treatment for chronic stable angina,
(2) - During treatment for chronic stable angina
(3) - Despite maximal antiischemic drug therapy

For Example
A patient with rest angina within 48 hrs with a defenite cardiac cause,not on treatment is classified as class III B 1