Cardiovascular hypertension

Some general principles for the treatment of Seronegative Spondylarthritis can be summarized as follows. Mild cases of SpA are controlled with physiotherapy and NSAIDs, paying attention to GI, renal, cardiovascular, hypertensive and hepatic risk... 

Cardiovascular Hypertension, congestive heart failure exacerbation... 

Pharmacologically, the ability (i) to selectively deliver dopamine to peripheral kidney receptors without eliciting complications due to the presence of dopamine receptors in the central nervous system (CNS) and (ii) to maintain a supply of nonmetabolized dopamine would be advantageous in cardiovascular hypertension therapy (6). The additional issues presented by this type of application include the dimensions of the dendrimer encapsulated dopamine and the targetting of the unit to the appropriate dopamine receptor sites. 

Cardiovascular hypertension is caused by either increased peripheral vascular resistance or increased cardiac output. The latter may be due to hyperthyroidism. The cause, however, is usually decreased elasticity of blood vessels with age that results in systolic pressure increases. Aortic constriction is occasionally at fault. 

Cardiovascular (hypertension) effects Hypertension, increased the risk for hypertensive heart disease and eerebrovaseular disease as latent effects... 

Cardiovascular Hypertension was common in a retrospective chart review of patients with colorectal cancers treated with bevacizumab 21% developed grade 3 hypertension, 14% grade 2 hypertension, and 7% grade 1 hypertension [89 ]. 

Fluid volume shifts Hyperkalemia Cardiovascular Hypertension Cardiomyopathy Immunological Increased risk of Infection Herpes zoster... 

Cardiovascular Hypertension Cardiac electrical function Cardiac calcium use Cardiac Na/K metabolism... 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

W. B. Kaimel and T. R. Dauber, Hypertensive Cardiovascular Disease The Framingham Study. Hypertension Mechanisms and Management, Framingham, Mass., 1973. 

Other Cardiovascular Agents Effecting Atherosclerosis. A large amount of clinical data is available concerning semm Upid profiles in patients subjected to dmg therapy for other cardiovascular diseases. Atheroma, for example, may be the underlying cause of hypertension and myocardial infarction. There are on the order of 1.5 million heart attacks pet year in the United States (155). 

Hypertension is one of the two principal risk factors of many cardiovascular diseases, such as coronary heart disease (CHD), stroke, and CHF. Individuals are considered hypertensive if their systoHc arterial blood pressure is over 140 mm Hg (18.7 Pa) or their diastoHc arterial blood pressure is over 90 mm Hg (12 Pa). Over 60 million people, or one-third of the adult population in the United States are estimated to be hypertensive (163). About 90% of these patients are classified as primary or essential hypertensive because the etiology of their hypertension is unknown. It is generally agreed that there is a very strong genetic or hereditary component to this disease. 

It is well accepted that hypertension is a multifactorial disease. Only about 10% of the hypertensive patients have secondary hypertension for which causes, ie, partial coarctation of the renal artery, pheochromacytoma, aldosteronism, hormonal imbalances, etc, are known. The hallmark of hypertension is an abnormally elevated total peripheral resistance. In most patients hypertension produces no serious symptoms particularly in the early phase of the disease. This is why hypertension is called a silent killer. However, prolonged suffering of high arterial blood pressure leads to end organ damage, causing stroke, myocardial infarction, and heart failure, etc. Adequate treatment of hypertension has been proven to decrease the incidence of cardiovascular morbidity and mortaUty and therefore prolong life (176—183). 

Treatment of essential or primary hypertension emphasizes not only the lowering of the elevated blood pressure, but also individualized therapy for each patient, providing each patient with minimized unnecessary side effects. The patient s cardiovascular morbidity and mortaUty should be decreased and end organ damage reversed or reduced (184,185). 

Hypokalemia. Hypokalemia associated with thia2ide diuretic therapy has been knpHcated in the increased incidence of cardiac arrhythmias and sudden death (82). Several large clinical trials have been conducted in which the effects of antihypertensive dmg therapy on the incidence of cardiovascular complications were studied. The antihypertensive regimen included diuretic therapy as the first dmg in a stepped care (SC) approach to lowering the blood pressure of hypertensive patients. 

One study (83) indicated that in mildly hypertensive male patients treated with an antihypertensive dmg, those below the age of 50 or having no clinical evidence of cardiovascular disease had no significant improvement from cardiovascular diseases within 3.3 years those over the age of 50 or having pre-existing cardiovascular disease benefited significantly. 

Another study (84), which enrolled men and women between the ages of 21—55 who had mild hypertension and no recognizable cardiovascular risk factors, showed no significant differences in mortaUty between dmg- and placebo-treated patients. Significant reductions in hypertensive complications were noted, but atherosclerotic complications were not reduced. 

A third study (85) enrolled 7825 hypertensive patients (55% males and 45% females) having diastoHc blood pressures (DBP) of 99—104 mm Hg (13—14 Pa) there were no placebo controls. Forty-six percent of the patients were assigned to SC antihypertensive dmg therapy, ie, step 1, chlorthaUdone step 2, reserpine [50-55-5] or methyldopa [555-30-6], and step 3, hydralazine [86-54-4]. Fifty-four percent of the patients were assigned to the usual care (UC) sources in the community. Significant reductions in DBP and in cardiovascular and noncardiovascular deaths were noted in both groups. In the SC group, deaths from ischemic heart disease increased 9%, and deaths from coronary heart disease (CHD) and acute myocardial infarctions were reduced 20 and 46%, respectively. 

When adrninistered long-term for the treatment of hypertension, diuretics fulfill the goals of preventing cardiovascular disease and increasing longevity. However, diuretic therapy may produce both side and toxic effects that are significant in certain patient subgroups, eg, diabetics and cardiac patients. 

NO is now recognized as a key neuro transmitter in humans and other animals and its biologically triggered synthesis is implicated in cardiovascular pharmacology, hypertension, impotence, immunology and other vital functions.NO and NO2 are important in... 

The so-called calcium channel blockers constitute a class of cardiovascular agents that have gained prominence in the past few years. These drugs, which obtund contraction of arterial vessels by preventing the movement of calcium ions needed for those contractions, have proved especially useful in the treatment of angina and hypertension. Dihydropyridines such as nifedipine (30) are par-... 

Dr. Kenneth Mukamal sfindings were published in January 2003. The news just gets better. A study whose Jindings were released in March 2004 suggested that moderate drinking not only had protective cardiovascular effects, but that it was also protective for people with hypertension. 

Angiotensin converting enzyme (ACE) plays a central role in cardiovascular hemostasis. Its major function is the generation of angiotensin (ANG) II from ANGI and the degradation of bradykinin. Both peptides have profound impact on the cardiovascular system and beyond. ACE inhibitors are used to decrease blood pressure in hypertensive patients, to improve cardiac function, and to reduce work load of the heart in patients with cardiac failure. 

---