Pulse pressure has implications for both cardiovascular disease as well as many non-cardiovascular diseases. Even in people without other risk factors for cardiovascular disease, a consistently wide pulse pressure remains a significant independent predictor of all-cause, cardiovascular, and, in particular, coronary mortality. There is a positive correlation between high pulse pressure and markers of inflammation, such as
c-reactive protein.
Cardiovascular disease and pulse pressure Awareness of the effects of pulse pressure on morbidity and mortality is lacking relative to the awareness of the effects of elevated systolic and diastolic blood pressure. However, pulse pressure has consistently been found to be a stronger independent predictor of cardiovascular events, especially in older populations, than has systolic, diastolic, or mean arterial pressure. This suggests that interventions that lower diastolic pressure without also lowering systolic pressure (and thus lowering pulse pressure) could actually be counterproductive. For such patients, it may be dangerous to target a peripheral systolic pressure below 120 mmHg due to the fact that this could cause the diastolic blood pressure in the cerebral cortex in the brain to become so low that perfusion (blood flow) is insufficient, leading to
white matter lesions. Nearly all coronary perfusion and more than half of cerebral perfusion occurs during diastole, thus a diastolic pressure that is too low can cause harm to both the heart and the brain. Increased pulse pressure is also a risk factor for the development of
atrial fibrillation.
Effects of medications on pulse pressure There are no drugs currently approved to lower pulse pressure. Although some anti-hypertensive drugs currently on the market may have the effect of modestly lowering pulse pressure, others may actually have the counterproductive effect of increasing pulse pressure. Among classes of drugs currently on the market, a 2020 review stated that
thiazide diuretics and long‐acting
nitrates are the two most effective at lowering pulse pressure. There is evidence that
glyceryl trinitrate, a nitric oxide donor, may be effective at lowering both pulse pressure and overall blood pressure in patients with acute and sub-acute stroke. A 2001 randomized, placebo-controlled trial of 1,292 males, compared the effects of
hydrochlorothiazide (a
thiazide diuretic),
atenolol (a
beta-blocker),
captopril (an
ACE inhibitor),
clonidine (a central
α-agonist),
diltiazem (a
calcium channel blocker), and
prazosin (an
α-blocker) on pulse pressure and found that, after one year of treatment, hydrochlorothiazide was the most effective at lowering pulse pressure, with an average decrease of 8.6 mmHg. Captopril and atenolol were equal as least effective, with an average decrease of 4.1 mmHg. Clonidine (decrease of 6.3 mmHg), diltiazem (decrease of 5.5 mmHg), and prazosin (decrease of 5.0 mmHg) were intermediate.
Pulse pressure and sepsis Diastolic blood pressure falls during the early stages of
sepsis, causing a widening of pulse pressure. If sepsis becomes severe and
hemodynamic compromise advances, the systolic pressure also decreases, causing a narrowing of pulse pressure. A pulse pressure of over 70 mmHg in patients with sepsis is correlated with an increased chance of survival. A widened pulse pressure is also correlated with an increased chance that someone with sepsis will benefit from and respond to
IV fluids. == See also ==