If this person exercises on a treadmill (or shovels snow, chops wood, digs a hole for a fence, or performs similar activity), his heart will need to pump twice as much blood to deliver twice as much oxygen to the muscles of the arms and legs. With 70% blockage of the coronary arteries, the heart muscle likely will not get the blood flow it needs. This may manifest as fatigue, shortness of breath, or discomfort in the chest or arms.

An unsuspecting person may attribute these symptoms to overexertion and will slow down or stop the exercise and never realize that is heart is producing warning signs. On a treadmill under continuous ECG monitoring, however, the ECG usually identifies the problem before a full-blown heart attack has occurred, it is hoped.
In cases of angina, when the blockage is temporary, the telltale ECG changes will be temporary as well. When a heart attack has occurred, on the other hand, a part of the actual heart muscle has died, and the ECG changes will be permanent.

In a heart attack, affected portion(s) of the heart will be electrically silent, and, like a burned-out light bulb, no longer radiate energy.

This shows up as changes in the voltages of the ECG, especially of the QRS complex.
For these reasons, it is especially important to go to a hospital emergency department in the early stages of a heart attack.

Some people are eligible to receive a medication that rapidly dissolves the coronary artery blockage.

This medication works only if it is given within 6 hours after the onset of symptoms.

Other people are not eligible to receive this medication because of potential complications, such as bleeding.
Electrical problems within the heart may disrupt the heart's natural pacemaker.

The extensive electrical network of nerves and nerve centers that coordinate the firing of the 4 chambers is made of living cells that require oxygen every bit as much as the heart muscle. These cells are subject to malfunction when starved of oxygen by blockage of a coronary artery. When this occurs, the heart may beat too fast, too slowly, or too irregularly to sustain its normal pumping function.
For example, if the coronary artery supplying the sinus node is blocked, the sinus node may fail. If the failure is partial, the heart rate will slow down. If the failure is complete, then there will be no activation of the atria, no atrial contraction, and no signal to trigger the AV node. The heart will stop pumping. This is called cardiac arrest and usually causes death.
Fortunately, the AV node has automaticity of its own. This means that in the absence of a normal incoming signal from the sinus node, the AV node will fire on its own, but at the slower rate of 35-60 times per minute.

Depending on the condition of the rest of the heart (the coronary arteries and the valves, for example), this slower rate may or may not result in symptoms.
Because a heart so affected loses its ability to speed up when needed, it is generally only a matter of time before the condition results in noticeable symptoms. This condition, known as sick sinus syndrome, is one of the more common reasons that people need an artificial pacemaker.
Sometimes a body's natural pacemaker malfunctions despite an otherwise perfectly healthy heart. (This is the equivalent to a car engine that doesn't run well because of a spark plug problem.) This was the situation for Arne Larsson, a Swedish engineer who received the first artificial pacemaker in 1958. He died in December 2001, aged 86 years, of causes unrelated to his heart.
Sometimes the heart's 2 ventricles beat so rapidly that very little or no blood at all is pumped because there is not enough time between contractions for the ventricles to fill.