Systolic and diastolic currents of injury

Why and How myocardial ischemia causes the ST segment changes?

Did you ask yourself this question before?

To answer such a question you need to go back to the physiological basics of electrocardiography. You must remeber that the ECG is the surface recording of electrical changes caused by electrical activity of the heart. At the culluar level those electrical changes are known as the action potential, which represents the potential differences across the cellular membrane as a result of a proper stimulus. The ischemia causes less negative resting membrane potential and loewr amplitude and longer duration of the action potential.



The ischemia is affecting a localized area and the rest of the myocardium is healthy and has normal action potential. This generates an electrical difference between the ischemic myocardium and the nearby healthy myocardium.

Systolic injury current:

During electrical systole (QT interval) the ischemic myocardium is less positive than the healthy myocardium (due to less amplitude of the action potential. This causes the electrical current to run from the healthy myocardium (more positive) to the ischemic myocardium. This is known as the systolic injury current. It is reflected in the ECG tracing as ST-segment elevation or depression according to the thickness and location of the ischemic area. If the ischemia affects the subendocardial area then the systolic injury current will be running from epicardium towards the endocardium (i.e. away from the body surface). The result will be ST-segment depression in the ECG leads corresponding to the ischemic territory. If the injuried area is whole thickness (transmural), then the systolic injury current will be running from the neighboring healthy myocardium towards the injured area. The summation vector of the resultant current will be directing outwards and causes ST-segment elevation in the leads representing the affected area.

Diastolic injury current:
The theory of diastolic current of injury is somewhat different. It is based on the fact that the resting membrane potential in the ischemic area is less negative in comparison with the healthy areas. This generates the diastolic injury current during the electrical diastole (TQ-interval). The direction of this current is from the ischemic area towards the healthy area. Thus it causes elevation of the TQ-segment in case of subendocardial infarction and depression of of TQ-segment in transmural infarction. But the TQ-segment is representing the base line for the ECG recording. So the net result will be apparent ST-segment depression and elevation respectively.


Images are from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.

Smoking paradox

Do you know about smoking paradox?

I first heard of this was during a clinical round a week ago. The professor asked us about it and nobody knew the answer. He told us the answer. It was noted that the incidence of in-stent stenosis following PCI was lower in smokers than non-smoker. He explained that by activation of CYP450 by smoking. This enzyme is responsible for transformation of clopidogrel to its active form. This lowers in-stent thrombosis and also lowered clopidogrel resistance.

However I have done my own search on the web to know more about that topic. I found some additional information. There are more explanations not mentioned by our professor. One explanation is the younger age of smokers in the studies revealing that paradox. Another one is the relectunce of smokers toseek medical advice when such problems occur. However, the long term mortality is still higher in smokers despite this claimed paradox.

I found two other paradoxes related to smoking. One was the lower mortality of somkers hospitalized for heart failure in OPIMIZE-HF study compared with non-smokers. However, the age of the smokers in the study was also younger, and this may be a resonable explanation. Another explanation is the difference in drug handling by smokers due to enzyme induction and inhibition. The third paradox related to smoking was noted in the study of lung cancer. It was noted the Japanese population has lower incidence of lung cancer compared with western populations, despite the higher incidence of smoking in the Japanese. This time the explanations were multiple. The main explanations were genetic difference, the different cigarette types and different filters, and the more healthy lifestyles led by the Japanese (less fat and less alcohol consumption).

The term "Paradox" may be deceiving or misleading. It gives the false impression that smoking is benfitial in this disease. The fact is exactly the opposite. Smoking causes the disease process to happen in an earlier age. And the real cause for the paradox is the younger age of the smokers, not the smoking itself, I guess. However it is still established that nonsmokers have longer and more healthy lives.

If you would like to read in more details follow these links:
1, 2 and 3.