Peripheral pulse pressure is the difference of the systolic blood pressure minus the diastolic blood pressure.  You want to keep the pulse pressure under 60.  A high pulse pressure is a measure of stiffness of the arteries.  A high pulse pressure is a risk factor for heart disease and premature death.

Systolic blood pressure and pulse pressure increase continuously throughout adult life and the prevalence of arterial hypertension rises accordingly, reaching 53-78% among those aged 65-74 years. Estimates of the prevalence of isolated systolic hypertension in the elderly range from 34-65%, with more women than men affected. It has been shown that within all age groups a difference in usual systolic blood pressure of 20 mm Hg or a difference in usual diastolic blood pressure of 10 mm Hg is associated with an approximately 2-fold difference in the risk of dying from stroke or ischemic heart disease.

Pulse Pressure Under 50 Best: The difference between systolic and diastolic blood pressure is a powerful independent predictor of cardiovascular disease over age 65. Systolic blood pressure rises with age due to stiffening of the arteries, while diastolic BP often remains constant or declines. A study followed 2,152 older adults with no evidence of heart problems. After ten years, 328 had had a heart attack or had died from heart disease, 224 had developed heart failure, and a total of 1,046 had died. For every 10–mm Hg increase in pulse pressure, the participants’ heart-disease risk increased by 12%, their risk of heart failure increased by 14%, and their mortality risk was raised by 6%. The data were adjusted for a number of variables, including smoking and other cardiac risk factors. Pulse pressure was most strongly linked to subsequent heart risk in the 600 participants who did not have any diagnosis of hypertension and who weren’t taking antihypertensives. They had a nearly 50% increase in CHD risk per 10–mm Hg increase in pulse pressure. J Am Coll Cardiol. 2000;36:130-8.

Keep Pulse Pressure Under 60: Pulse pressure (PP) greater than 60 mm Hg is an independent predictor of cardiovascular (CV) risk. In a 9-month open study of 1841 primary care physicians treating 6110 hypertensive patients who had a baseline PP >60 mm Hg and were divided into five antihypertensive therapy categories: 1) no antihypertensive therapy; 2) antihypertensive therapy incorporating neither an angiotensin-converting enzyme inhibitor (ACEI) nor a diuretic; 3) ACEI but no diuretic; 4) diuretic but no ACEI; and 5) ACEI + diuretic. In each category, any other antihypertensive agent could be added to lower the PP below 60 mm Hg. At 9 months, 95% of patients were receiving the ACEI + diuretic combination versus <10% at inclusion. During this period PP decreased below 60 mm Hg in 48% of the patients, and persisted above 80 mm Hg in less than 5%. New CV events occurred in 221 patients and were predicted by a positive CV history and age <50 years (odds ratio [OR]: 2.49). In patients without a CV history, the only predictor of decreased CV events was ACEI + diuretic combination (OR: 0.50). In the overall population, age <50 years and PP <60 mm Hg predicted a lack of new CV events (OR: 0.55). Pulse pressure monitoring of open antihypertensive therapy. Safar ME, Vaisse B, et al. Hopital Hotel Dieu, Paris, France. Am J Hypertens. 2004 Dec;17(12 Pt 1):1088-94

Atrial Fibrillation Higher with Increased Pulse Pressure: In 5331 Framingham Heart Study participants over age 34 and initially free from AF (median age, 57), AF developed in 698 participants (13%) a median of 12 years after pulse pressure assessment. Cumulative 20-year AF incidence rates were 5.6% for pulse pressure of 40 mm Hg or less (25th percentile) and 23.3% for pulse pressure greater than 61 mm Hg (75th percentile). In multivariate analysis, pulse pressure was associated with increased risk for AF (HR: 1.26 per 20-mm Hg increment; P<.001). In contrast, mean arterial pressure was unrelated to incident AF. Systolic pressure was related to AF (HR, 1.14 per 20-mm Hg increment; P = .006). Pulse pressure and risk of new-onset atrial fibrillation. Mitchell GF, et al. Waltham, Mass. . JAMA 2007 Feb 21;297(7):709-15.

Pulse Pressure Heart Failure Risk Factor: In a 24-year follow-up of 2040 Framingham adults average age 61, 234 developed heart failure, systolic BP and pulse pressure were more important risk factors than diastolic BP. A 1-SD (20 mm Hg) increment in systolic pressure conferred a 56% increased risk; a 1-SD (16 mm Hg) increment in pulse pressure conferred a 55% increased risk for CHF. Increased pulse pressure may help identify hypertensive patients at high risk for overt CHF who are candidates for aggressive blood pressure control. Haider AW et al. Ann Intern Med. 2003 Jan 7;138(1):10-6.

Low Pulse Pressure Bad in Those Already Having Heart Failure: In 8660 patients with heart failure, after 1 year, 11.5% died. Both the mean arterial pressure and systolic blood pressure were found to be inversely associated with mortality at univariate and multivariate analyses. An inverse univariate relation was observed between PP and all-cause mortality. An excess mortality risk in the lowest PP group (odds ratio 1.40 vs the highest PP group) in a multivariate analysis. For any given level of mean arterial pressure, a low PP is an independent predictor of all-cause and cardiovascular death in patients with heart failure. A low pulse pressure is an independent predictor of mortality in heart failure: data from a large nationwide cardiology database (IN-CHF Registry). Schillaci G, Di Luzio S, et al. University of Perugia, Italy. Ital Heart J. 2004 Dec;5(12):892-8.

Peripheral Pulse Pressure Shortcomings with Slow Pulse: Peripheral pulse pressure does not always provide a reliable measure of changes in central pulse pressure or arterial stiffness. Twenty adults ages 20-72 years were studied at cardiac catheterization with right atrial pacing (80 to 120 beats/min). Pulse pressure amplification increased during pacing due to a reduction in central pressure augmentation. Augmentation Index (Aix) was significantly and inversely related to heart rate (r = -0.70, P < .001) due to an alteration in the relative timing of the reflected pressure wave, rather than a reduction in arterial stiffness, as PWV did not change. Heart rate dependency of pulse pressure amplification and arterial stiffness. Wilkinson IB, Mohammad NH, et al., University of Edinburgh, Am J Hypertens. 2002 Jan;15(1 Pt 1):24-30.

Pulse Pressure Valuable Measure in Heart Disease: In a study 110 patients with coronary artery disease, only 24-h pulse pressure was significantly related to the severity of coronary artery disease (P < .01), carotid IMT (P < .01), and left ventricular (LV) mass index (P < .01). In a multivariate analysis, 24-h pulse pressure was also the best predictor of the severity of coronary lesions (P = .009), carotid IMT (P = .003), and LV mass index (P = .009). Zakopoulos NA, et al. Athens Univ. Am J Hypertens. 2001 Mar;14(3):195-9.

Pulse Pressure Predictor of Heart Disease Only After Age 50: In a 20-year follow-up of 6539 adults ages 20-79 free of CHD at onset, in the group under 50 years of age, DBP was the strongest predictor of CHD risk (HR per 10 mm Hg increment, 1.34) rather than SBP (HR, 1.14) or PP (HR, 1.02). Between 50 to 59 years of age, risks were comparable for all 3 BP indexes. In the older age group, the strongest predictor of CHD risk was PP (HR, 1.24). When both SBP and DBP were considered jointly, the former was directly and the latter was inversely related to CHD risk in the oldest age group. Does the relation of blood pressure to coronary heart disease risk change with aging? The Framingham Heart Study. Franklin SS, Larson MG, et al, University of California, Circulation. 2001 Mar 6;103(9):1245-9.

Gene Polymorphism Related to High Pulse Pressure: In the three genotypes of the plasminogen activator inhibitor (PAI)-1 gene polymorphism, the gender-adjusted difference in the relationships between age and PP in subjects with never treated essential hypertension found that the genotype deletion (D)/D at position -675 of the PAI-1 insertion (I)/D gene polymorphism was associated with a significant increase in the adjusted slope of the curve relating age to PP by comparison with the two other genotypes. No comparable difference in age-related changes in systolic, diastolic or mean blood pressure was found. Age-related increase of pulse pressure and plasminogen activator inhibitor-1 I/D gene polymorphism in essential hypertension. Mourad J-J, du Cailar G, et al. Hotel Dieu Hospital, Paris, France. J Intern Med 2005; 257: 93-99.

Pulse Pressure as Good as Systolic Blood Pressure Predicting Heart Attacks, Strokes, Death: In a 7-year follow-up study of 4,234 Rotterdam adults aged 55 and older with no previous myocardial infarction (MI) or stroke, 205 had a heart attack (MI), 137 a stroke, and 748 died. A 1-standard deviation difference in SBP, DBP, and PP was associated with relative risks of MI of 1.24, 1.07, and 1.25. Corresponding relative risks for stroke were 1.59, 1.27, and 1.48. For all-cause mortality the corresponding relative risks were 1.21, 1.06, and 1.20. Blood pressure components and cardiovascular events in older adults: the Rotterdam study. Mattace-Raso FU, van der Cammen TJ, et al. Erasmus Medical Center, Rotterdam, the Netherlands. J Am Geriatr Soc. 2004 Sep;52(9):1538-42

Genes Big Factor in Pulse Pressure: Researchers

Renal Damage Can Lead to Hypertension and Arterial Stiffness: Microalbuminuria is an early marker of renal damage and predicts future cardiovascular mortality and morbidity in patients with diabetes or hypertension, as well as people in general. In a study of 136 adults with no cardiovascular diseases except for hypertension and who were not taking any medications, urinary albumin concentration was determined by the standard method and corrected by creatinine. Microalbuminuria was defined as a urinary albumin/creatinine ratio of 2.0-30.0 mg/mmol creatinine. Individuals with microalbuminuria had higher blood pressure and wider pulse pressure. Microalbuminuria was associated with significantly higher pulse wave velocity compared with that of normoalbuminuric individuals: average PWV: 821 cm/s vs. 934 cm/s, p<0.0001). Stepwise regression analysis revealed that the presence of mircroalbuminuria (p=0.047) was a significant independent predictor of PWV in addition to age, sex, and systolic blood pressure. This suggests that microalbuminuria is associated with advanced atherosclerosis in the general population. Underlying arterial stiffness may explain the high cardiovascular mortality in subjects with microalbuminuria. Hypertension may be the mechanism linking microalbuminuria and arterial stiffness in the general population. Microalbuminuria and arterial stiffness in a general population: the Shimanami Health Promoting Program (J-SHIPP) study. Kohara K, Tabara Y, et al. Ehime University, Japan. Hypertens Res. 2004 Jul;27(7):471-7

Danger of Low Diastolic Blood Pressure Only in Those with Systolic Hypertension: By prospectively testing in the combined original and offspring Framingham cohorts, researchers confirmed that the increase in cardiovascular disease (CVD) incidence at low diastolic blood pressure (BP) is largely confined to subjects with increased systolic BP and hence an increased pulse pressure. The 10-year risk of 951 nonfatal CVD events and 204 CVD deaths was estimated at diastolic pressures of <80, 80 to 90, and > or =90 mm Hg, according to concomitant systolic BP. An increasing tendency for a J-curve relation of CVD incidence to diastolic BP was observed with successive increments in accompanying systolic BP. In both genders, a statistically significant excess of CVD events was observed at a diastolic BP of <80 mm Hg only when accompanied by a systolic BP of >140 mm Hg that persisted after adjustment for age and associated CVD risk factors. A likely explanation for the J-curve of blood pressure cardiovascular risk. Kannel WB, Wilson PW, et al. Boston University  Am J Cardiol. 2004 Aug 1;94(3):380-4

Early Treatment Best: In the 6-year DB PC Systolic Hypertension in Europe (Syst-Eur) trial, 4695 adults over age 59 with untreated blood pressure of 160-219 mmHg systolic and below 95 mmHg diastolic were first treated for 2 years with placebo or nitrendipine (10-40 mg daily) with the possible addition of enalapril (5-20 mg daily), hydrochlorothiazide (12.5-25 mg daily), or both add-on drugs. Systolic pressure decreased to below 150 mmHg (target level) in 75.0%. During the 4-year open-label follow-up, stroke and cardiovascular complications occurred at similar frequencies in patients formerly randomized to placebo and those continuing active treatment. These rates were similar to those previously observed in the active-treatment group during the double-blind trial. Considering the total follow-up of 4695 randomized patients, immediate compared with delayed antihypertensive treatment reduced the occurrence of stroke and cardiovascular complications by 28% (P = 0.01) and 15% (P = 0.03), respectively, with a similar tendency for total mortality (13%, P = 0.09).

Thomas E. Radecki, M.D., J.D.

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