Communicating with patients about their medications.
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Drug Therapy↗
Biomedical subjects
C V Ram
Publications and source records attributed to C V Ram.
Current concepts in renovascular hypertension.
Renovascular disease represents an important dimension of hypertension. Although estimates vary regarding the exact prevalence of renovascular hypertension, it is being diagnosed with increasing frequency because of refined criteria for the workup and the availability of sensitive diagnostic tests. Two major pathologic entities--atherosclerosis and fibromuscular dysplasia--account for most cases of renovascular hypertension. Once the diagnosis and clinical significance of renal artery stenosis in a hypertensive patient are established, appropriate and specific therapy should be considered. The goal is not only to treat hypertension, but to preserve and restore renal function. Although antihypertensive drug therapy may lower the blood pressure, reperfusion of the kidney (surgical, angioplasty) is a desirable long-term objective in the management of patients with renovascular hypertension. With careful selection of therapeutic choices, we are now able to render optimal care to patients with renovascular hypertension.
Animals↗
Management of hypertensive emergencies: changing therapeutic options.
Rapid lowering of severe hypertension is essential to prevent irreversible damage to vital organs. The patient's clinical status should be evaluated, noting particularly cardiac, neurologic, and renal functions. Choice of treatment should be based on speed and efficacy of action and on hemodynamic, vascular, and renal consequences. It is also important to preserve circulatory homeostasis and vital organ function. Sodium nitroprusside, labetalol, diazoxide, and hydralazine have been used parenterally for rapid control of severe hypertension, but they do not always produce optimal, balanced hemodynamic effects. Calcium antagonists have been advocated because of their beneficial circulatory effects. Nicardipine, a new dihydropyridine calcium antagonist, produces significant antihypertensive effects, and when given intravenously, results in a rapid fall in blood pressure. Studies have confirmed that nicardipine is effective and safe in the management of severe hypertension and hypertensive crises. Because the aim of rapidly controlling severe hypertension is to prevent target organ dysfunction, nicardipine therapy offers a useful additional option in the clinical management of severe hypertension and hypertensive crises.
Emergencies↗
Hypertension and atherosclerosis.
Sufficient evidence exists to implicate hypertension as a potent independent risk factor for the development of atherosclerosis. Whereas certain biochemical pathways may play some role in the genesis of atherosclerosis in patients with hypertension, the blood pressure level alone may accelerate the atherosclerotic process. This article discusses the link between hypertension, atherosclerosis, and antihypertensive therapy.
Antihypertensive Agents↗
Anti-atherosclerotic and vasculoprotective actions of calcium antagonists.
Treatment of hypertension may prevent many of the complications attributable to blood pressure elevation, particularly those that are "pressure-related," such as stroke. However, the atherosclerotic complications of hypertension, e.g., coronary artery disease manifested as coronary morbidity and mortality, have not been reduced significantly with antihypertensive therapy. This disappointing outcome may reflect the adverse metabolic effects of the traditional therapies, diuretics and beta blockers, and their lack of specific vasoprotective properties. Increasing attention is thus being paid to the newer antihypertensive agents, which typically have fewer adverse effects and perhaps more physiologic mechanisms of antihypertensive action. Since calcium plays a key role in the genesis of atherosclerosis, calcium antagonists may positively affect the course of vascular disease. Investigators have observed that calcium antagonists display clear antiatherosclerotic properties in experimental as well as clinical studies. In one recently published clinical study, coronary artery disease was shown to develop more slowly, with a slower progression of individual stenoses, higher regression rate and less frequent occurrence of new lesions in patients treated chronically with verapamil compared to those receiving conventional therapies. Other similar investigations are currently under way to evaluate the antiatherogenic properties of calcium antagonists, including the Frankfurt Isoptin Progression Study (FIPS), the Multicenter Isradipine Diuretic Atherosclerosis Study (MIDAS), the International Nifedipine Trial on Atherosclerosis Coronary Therapy (INTACT), and the large-scale Montreal Heart Institute Study. Results of these studies, which use precise end points such as myocardial infarction, cerebral infarction and peripheral vascular disease, may revolutionize the treatment of hypertension by identifying therapeutic approaches that control both the pressure-related and atherosclerotic complications of the disease.
Antihypertensive Agents↗
Potassium supplements for hypertension.
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Diet, Sodium-Restricted↗
Nicardipine and propranolol in the treatment of hypertension: similar antihypertensive but dissimilar hemodynamic actions.
Although the precise cause of essential hypertension is not known, empiric treatment is indicated to reduce cardiovascular risks. Several pharmacologic classes of a antihypertensive drugs are available to reduce blood pressure, but they do so by different hemodynamic mechanisms. The physiologic therapeutic goal in patients with hypertension is to normalize the systemic vascular resistance without inducing major alterations in the cardiac output. In this study we compared the antihypertensive and hemodynamic actions of nicardipine, a calcium antagonist, with propranolol, a beta-blocking drug. Both drugs were effective in the treatment of hypertension. However, while propranolol therapy decreased the resting and exercise left ventricular ejection fraction and cardiac output, cardiac function was well preserved during nicardipine therapy. It is concluded that both nicardipine and propranolol exert similar antihypertensive actions but that they cause dissimilar hemodynamic consequences in patients with uncomplicated hypertension.
Antihypertensive Agents↗
Current concepts in the diagnosis and management of hypertensive urgencies and emergencies.
Hypertensive crises constitute a group of distinct clinico-pathological entities in which rapid control of hypertension is indicated to previous serious complications. Although systemic blood pressure is invariably elevated in these conditions, it is the status of the target organ function which determines the need for urgent reduction of blood pressure. The physicians should be cognizant of the pathophysiological basis of hypertensive crises so that rational therapeutic choices can be made. The chief objective should be to arrest and, if possible, to reverse the target organ damage. Once the diagnosis of hypertensive crisis is evident, the blood pressure should be lowered quickly while paying careful attention to the cardiovascular, neurologic, and renal function. Several potent, parentally effective antihypertensive drugs such as nitroprusside, labetalol, and nicardipine are available to produce an immediate fall in blood pressure. The choice of drug therapy should be made on the basis of the pharmacodynamic and clinical effects, advantages, and disadvantages. Once the emergency situation is resolved, the etiology of hypertensive crisis should be considered.
Antihypertensive Agents↗
Antiatherosclerotic and vasculoprotective effects of calcium antagonists: clinical implications.
Clinical experience and epidemiological observations have demonstrated that some hypertensive patients experience progression of atherosclerotic vascular disease despite successful control of hypertension. Thus, there appears to be a discordance relative to the benefits of antihypertensive therapy--'pressure'-related but not 'atherosclerotic' complications are prevented by BP control with conventional antihypertensive therapy. The effects of antihypertensive drugs on atherosclerotic complications of hypertension is a subject of major clinical importance. The question is whether or not different classes of antihypertensive drugs exert dissimilar vasculoprotective actions independent of their BP lowering effects. There is considerable experimental data to implicate a relationship between calcium and lipoprotein metabolism at the vascular site. The calcium ion may play a role in the steps culminating in the formation of atherosclerotic plaques. Evidence has been presented that calcium channel blockers may modify experimental arterial calcinosis and atherosclerosis. At least a couple of published trials have shown that calcium antagonists indeed prevent/attenuate atherosclerotic lesions in patients with coronary artery disease. These observations underscore the significance of a new dimension in cardiovascular drug therapy--that is the vasculoprotective and antiatherosclerotic effects of calcium antagonists.
Arteriosclerosis↗
Regression of left ventricular hypertrophy in hypertension. Effects of prazosin therapy.
Left ventricular hypertrophy is a common consequence of chronic hypertension. Although the hypertrophic response can be considered an adaptive mechanism in the initial stages, its progression is associated with increased cardiovascular morbidity and mortality rates. Therefore, reversal of left ventricular hypertrophy may provide considerable clinical benefits to hypertensive patients. Although treatment of hypertension per se is important, blood pressure alone may not explain the course of the hypertrophic process. Not all antihypertensive drugs cause a reversal of hypertrophy, though they may produce equal effects on blood pressure. Factors other than the severity of blood pressure may play a role in the genesis of left ventricular hypertrophy. Adrenergic inhibitors cause its regression, whereas direct vasodilators may promote progression. In this study, therapy with the alpha-adrenergic inhibitor prazosin resulted in significant regression of left ventricular hypertrophy in a group of patients with moderate-to-severe hypertension. This study utilized a new technique--[123I]phenylpentadecanoic acid myocardioscintigraphy--to measure the left ventricular mass. In this study, it was shown that monotherapy with prazosin produced significant relative reductions in systolic and diastolic blood pressure, along with significant reductions in left ventricular mass.
Blood Pressure↗
Nicardipine and propranolol in the treatment of essential hypertension.
Two hundred thirty-four patients with supine diastolic blood pressure of between 95 and 114 mm Hg were enrolled into a double-blind, randomized, parallel, multicenter trial. The patients were randomized to either nicardipine 30 mg tid, propranolol 40 mg tid, or nicardipine 30 mg tid and propranolol 40 mg tid for six weeks. Two hundred six patients yielded data for analyses. Of the 28 not included, seven had missing data, whereas the remaining 21 were excluded because they either failed to meet inclusion criteria or were noncompliant at endpoint. Both nicardipine and propranolol as monotherapies and in combination achieved statistically significant, (P less than .01), supine diastolic blood pressure reduction relative to baseline. The combination of nicardipine and propranolol showed a greater reduction in supine diastolic and systolic measurements than either of the monotherapies. Nicardipine produced greater blood pressure reductions one hour after dosing, whereas the propranolol treatment tended to produce slightly greater blood pressure decreases eight hours after dose. The combination always resulted in the greatest blood pressure reduction, independent of time after dose. Adverse experiences were reported by 26% of patients in the nicardipine-treated group, most often transient vasodilatory effects, by 17% of the propranolol-treated patients, and by 18% of the combination-treated group. This study demonstrated at the doses studied that nicardipine alone produced equivalent blood pressure reductions to those obtained by propranolol alone, but that the combination of these two drugs produced greater reductions in blood pressures than either of the monotherapies.
Adult↗
Regression of left ventricular hypertrophy in hypertension with alpha-adrenergic blockade: physiological basis and therapeutic implications.
Left ventricular hypertrophy may be a serious consequence of chronic untreated hypertension since it may accentuate the risk of congestive heart failure, arrhythmias, coronary ischaemias and sudden death. Although haemodynamic factors may play a role in the genesis of left ventricular hypertrophy, certain neurohumoral mechanisms such as the adrenergic nervous system may induce left ventricular hypertrophy in patients with hypertension. There is considerable evidence to implicate adrenergic activation in the pathogenesis of left ventricular hypertrophy. Thus, adrenergic blockade may have a favourable impact on the course of left ventricular hypertrophy. Recent studies discussed in this paper have demonstrated that postsynaptic alpha-adrenergic blockers cause a significant reduction in the left ventricular mass. It is concluded that alpha-adrenergic blockers can be added to the list of antihypertensive drugs which can cause regression of left ventricular hypertrophy in patients with hypertension.
Adrenergic beta-Antagonists↗
Intravenous nicardipine for the treatment of severe hypertension. A double-blind, placebo-controlled multicenter trial.
A placebo-controlled, double-blind multicenter trial was conducted in 123 patients with severe hypertension to examine the efficacy and safety of intravenously administered nicardipine hydrochloride in controlling blood pressure. Seventy-three patients were initially randomized to receive nicardipine treatment. This group had an initial blood pressure of 213 +/- 3/126 +/- 2 mm Hg. Sixty-seven patients achieved the therapeutic goal (diastolic blood pressure less than or equal to 95 mm Hg; systolic blood pressure less than or equal to 160 mm Hg). Fifty patients were randomized to receive placebo solution. Blood pressure in these patients was 216 +/- 3/125 +/- 2 mm Hg. No patient in this group achieved the therapeutic goal during the "blinded" portion of the study. Forty-four of 49 patients who did not respond to placebo administration responded to subsequent treatment with nicardipine. Patients with end-organ damage were included in the study. These included patients with left ventricular hypertrophy, retinopathy, and renal insufficiency. Patients with and without end-organ damage responded equally well to nicardipine treatment. Serious adverse experiences were infrequent, the most common adverse reaction being headache in 24% of the patients studied.
Dose-Response Relationship, Drug↗
Ketanserin in essential hypertension. Effects of blood pressure on renal hemodynamics.
Essential hypertension is a multifactorial disorder mediated by multiple mechanisms. Serotonin may cause vasoconstriction either directly or indirectly by amplifying the actions of vasoconstrictor substances. Clinical trials indicate that ketanserin, a serotonin antagonist, is effective in treating hypertension. It is desirable for an antihypertensive agent to enhance or preserve renal hemodynamic function. In this study, we evaluated the acute (1 week) and chronic (8 weeks) effects of ketanserin (20-40 mg twice a day) on glomerular filtration rate, renal plasma flow, and sodium excretion in patients with uncomplicated hypertension. Patients with untreated diastolic blood pressure (greater than 90 mm Hg) received either ketanserin or a placebo during an 8-week double-blind trial. Findings demonstrated that patients treated with ketanserin showed an increase in renal plasma flow compared with those who received placebo. Sodium excretion remained unchanged, indicating the absence of sodium retention during therapy. These results show that ketanserin lowers blood pressure in essential hypertension while preserving renal hemodynamics and function.
Animals↗
Double-blind comparison of amlodipine and hydrochlorothiazide in patients with mild to moderate hypertension.
Amlodipine, a new long-acting dihydropyridine calcium antagonist, was compared with hydrochlorothiazie (HCTZ) in 145 patients with mild to moderate hypertension. After 4 weeks of single-blind placebo runin, patients were randomly allocated to receive amlodipine (2.5-10 mg once daily, n = 97) or HCTZ (25-100 mg once daily, n = 48). At study week 12 response rates for amlodipine and HCTZ were 61.5 and 60.5%, respectively. There were clinically significant reductions in 24-h postdose blood pressures with both amlodipine (-18/-11 mm Hg supine: -14/-10 mm Hg standing) and HCTZ (-18/-10 mm Hg supine, -18/-9 mm Hg standing). After study week 12, atenolol (50-100 mg once daily) was added to the regimen of those patients whose hypertension was not controlled with monotherapy. Neither amlodipine nor HCTZ produced clinically significant changes in pulse rate, electrocardiogram, or chest x-ray film. Although amlodipine increased and HCTZ decreased the high-density lipoprotein (HDL)/total cholesterol ratio and the HDL/(low-density lipoprotein + very-low-density lipoprotein) ratio, the difference between the two treatments was not statistically significant. The incidence of side effects and the rate of patient withdrawal was comparable in the two groups. The incidence of laboratory abnormalities was 56% with HCTZ (mainly hypokalemia and hyperuricemia) and 16% with amlodipine. Amlodipine was an effective, well-tolerated agent for treatment of mild-to-moderate hypertension in this study, as single-daily-dose monotherapy and in combination with atenolol.
Adolescent↗
New approaches for the treatment of hypertensive urgencies and emergencies.
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Antihypertensive Agents↗
Renovascular hypertension.
Renovascular hypertension is the most prevalent form of curable hypertension. Despite some unanswered questions, there is a growing consensus about the need to identify patients with renovascular hypertension so that a specific therapy can be recommended. The renin-angiotensin system is the chief pathophysiologic mechanism responsible for hypertension in patients with renal ischemia but other, yet poorly defined, mechanisms may be operative. Most patients with renovascular hypertension do not present with typical or discriminative clinical features. Thus, many physicians do not perform work-up to uncover renovascular disease even if diagnosis is dictated by patients' clinical course. It is difficult to make the proper diagnosis unless there is a high index of suspicion and certain procedures are performed. How can we, then, select a few patients for the work-up from the vast sea of people with hypertension? The identification of such patients and the pursuit of a renovascular etiology is a matter of clinical judgment. Delineation of renovascular hypertension should be undertaken only after careful deliberation. When clinical clues suggestive of renovascular hypertension are present, appropriate diagnostic tests should be undertaken in patients who are candidates for PTRA or surgery. Captopril-stimulated PRA test is done first. If the test is positive (and in some clinically relevant circumstances even if it is not done or is negative), DSA should be obtained. IV-DSA is being steadily replaced by the superior IA-DSA. The need for renal vein renin determination varies from center to center, but when carefully performed, it yields meaningful information. Ultimately, a conventional arteriogram is done to define the extent of renal artery stenosis and to assess intrarenal vascular anatomy. For selected patients, the benefit-risk ratio clearly outweighs the cost considerations. The spectrum of renovascular hypertension is variable, further compounding the diagnostic indications and contraindications. At one end of this spectrum are those patients in whom surgical therapy is likely to be beneficial, and at the other end are the patients who have relative contraindications to surgery. In between lies the vast gray zone that constitutes a great judgmental challenge in clinical medicine. What is to be done with the patients who have mild to moderate renovascular hypertension whose BP is controlled on medical therapy? There are some patients who may benefit from renovascular repair despite the nonlateralization of renal vein renins. What is the mechanism underlying their hypertension?(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Pheochromocytoma.
Although pheochromocytoma is an uncommon cause of secondary hypertension, it is also a curable form of hypertension. With proper treatment, the outlook for patients with pheochromocytoma is excellent. If undiagnosed or untreated, pheochromocytoma causes serious complications and death. The key to reaching the diagnosis is a high index of suspicion coupled with careful clinical evaluation and laboratory testing. Our ability to diagnose and localize pheochromocytoma has improved vastly, owing largely to the modern biochemical and radiologic techniques. Despite this, a number of pheochromocytomas remain undiagnosed only to be uncovered after a serious complication or at postmortem. The diverse manifestations and problems presented by patients with pheochromocytoma can be managed only with combined medical and surgical expertise, with assistance from our colleagues from the radiology and anesthesiology disciplines. Although sporadic pheochromocytoma is the most common form of presentation, the overall clinical picture may depend on the subset of affected individual--childhood, pregnancy, associated MEN, and neurocutaneous syndromes. Fortunately, more than 90 per cent of all pheochromocytomas originate in the adrenal gland, but the tumor can occur at any site in the sympathetic chain. The spectrum of clinical manifestations is so wide that a pheochromocytoma may mimic a variety of common disorders. It is as challenging to diagnose what is not a pheochromocytoma as it is to confirm its diagnosis. Surgical removal of pheochromocytoma is the treatment of choice. With proper preoperative medical management aimed at blocking the effects of catecholamines, operative mortality should be close to zero. For patients with inoperable, malignant, recurrent, or multicentric pheochromocytomas, chronic medical therapy is indicated in the form of alpha- and/or beta-blockade or inhibition of catecholamine synthesis with alpha-methyl-para-tyrosine. An understanding of the pathophysiology and natural course is vital to the rational management of patients with pheochromocytoma.
Humans↗