Systolic hypertension is lighter than Diastolic hypertension. In Diastolic hypertension, the diastolic blood pressure when the heart is relaxing is higher than normal means less blood will be received by the heart and makes higher heart beat (tired).
Systolic hypertension may be due to reduced compliance physiology of the aorta with increasing age. This increases the load on the ventricle and compromises coronary blood flow, eventually resulting in left ventricular hypertrophy, coronary ischemia, and heart failure.
Contemporary science shows an immersed boundary method of computational illustration of a single heartbeat. Applied to physiologic models, immersed boundary theory sees the heart as a great folded semisolid sail fielding and retrieving a viscous blood mass. The sail, likened to Windkessel effect physiology, gives and receives a load under time-ordered phases. Decreasing compliance of the sail heralds the onset of systolic hypertension.
The goal of treating systolic hypertension is to delay and reduce the extent of damage to the heart, the cerebrovascular system, and the kidneys. Lifestyle interventions are a crucial element of successful treatment, including a diet low in sodium (salt) and rich in whole grains, fruits, and vegetables. Clinical trials have also documented the beneficial effects of weight loss, increased physical activity, and limiting alcohol consumption.
In addition to lifestyle changes, medication can also be used to reduce systolic hypertension to safe levels, although medications frequently have side effects, often serious. Two randomized controlled trials have established the value of treating systolic hypertension:
1st: SHEP study
- Patients: inclusion criteria were SBP greater than 160 to 219 mm Hg and DBP less than 90 mm Hg. The mean initial blood pressure was 170/77.
- Treatment goal: 20 mmHg reduction in systolic pressure or a systolic pressure of less than 160 mmHg, whichever was lower
- Mean final blood pressure in the treatment group: 143/68
2nd: Syst-Eur Trial
- Patients: inclusion criteria were systolic of 160–219 mm Hg and diastolic blood pressure lower than 95 mm Hg. The average was 174/86.
- Treatment goal: "We aimed to reduce the sitting systolic blood pressure by at least 20 mm Hg to less than 150 mm Hg"
- Mean final blood pressure in the treatment group was 151/79; 44% of patients reached the target blood pressure goals.
The treatment goal
Based on these studies, treating to a systolic blood pressure of 140, as long as the diastolic blood pressure is 68 or more, seems safe. Corroborating this, a reanalysis of the SHEP data suggests allowing the diastolic to go below 70 may increase adverse effects.
A meta-analysis of individual patient data from randomized controlled trials found the nadir diastolic blood pressure below which cardiovascular outcomes increase is 85 mm Hg for untreated hypertensives and 80 mm Hg for treated hypertensives. The authors concluded "poor health conditions leading to low blood pressure and an increased risk for death probably explain the J-shaped curve". Interpreting the meta-analysis is difficult, but avoiding a diastolic blood pressure below 68–70 mm Hg seems reasonable because:
- The nadir value of 85 mm Hg for treated hypertensives in the meta-analysis is higher than the value of 68–70 mm Hg that is the nadir suggested by the two major randomized controlled trials of isolated systolic hypertension
- The two largest trials in the meta-analysis, Hypertension Detection and Follow-up Program (HDFP) and Medical Research Council trial in mild hypertension (MRC1) were predominantly middle-aged subjects, all of whom had diastolic hypertension before treatment.
- The independent contributions of diseases and factors other than hypertension versus effects of treatment are not clear in the meta-analysis.
Newer treatments have emerged since these trials, which address the underlying causes of hypertension in novel ways. For instance, a direct inhibitor of the kidney hormone renin, called aliskiren, has recently been released in the United States. It has antihypertensive efficacy similar to ACE inhibitors and angiotensin receptor blockers. By suppressing renin activity directly rather than indirectly (as these other medications do), it avoids a rebound in renin levels that gradually interferes with their efficacy. Over the long term, though, it may lead to increases in the physiological precursor of renin. Its role as a single agent without the concomitant use of other antihypertensives is not yet clear.
Medications that act on the sympathetic nervous system, which is important in the cause of hypertension, also show promise. European studies show selective imidazoline agonists, such as moxonidine and rilmenidine, are reasonably effective against hypertension while improving glucose tolerance and lipid metabolism.
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