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Biomedical subjects

M S Kochar

Publications and source records attributed to M S Kochar.

At least 19 recordsLinked to original sources
PubMed2000

The need to lower systolic blood pressure.

Systolic hypertension is the most common form of hypertension, especially in individuals aged 60 years or older. Systolic hypertension is a reflection of decreasing compliance of large arteries and is a strong independent risk factor for all cardiovascular diseases. Despite proven benefits of therapy for systolic hypertension, only 25% of patients with this condition are adequately treated to attain target blood pressures. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of high blood pressure (JNC VI) recommends the use of diuretics and long-acting dihydropyridine calcium channel blockers as first-line therapy for isolated systolic hypertension. Therapy is also guided by comorbid conditions where certain drugs may have additional benefits. The goal of therapy should be a graded reduction in blood pressure to less than 140/90 mm Hg with lower blood pressure targets in patients with coexistent diabetes or renal failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Management of postural hypotension.

Several mechanisms counteract the gravitational forces on blood and maintain systemic arterial pressure and cerebral perfusion upon assumption of the upright posture. Failure of these mechanisms can lead to a postural decrease in blood pressure. Postural hypotension is defined as a reduction of at least 20 mm Hg in systolic blood pressure or at least a 10 mm Hg decrease in diastolic blood pressure. Acute postural hypotension is usually due to fluid or blood loss and responds well to fluid repletion. Chronic postural hypotension is due to drugs or endocrine or neurogenic disorders. A functional classification based on severity of symptoms is useful in monitoring the patient's condition and documenting improvement with treatment. Whenever possible, the reversible causes of chronic postural hypotension should be treated. For symptomatic treatment, a stepped approach starting with nonpharmacologic measures is recommended. Fludrocortisone, midodrine, indomethacin, and atrial tachypacing are recommended, in that order, for patients in whom nonpharmacologic measures prove insufficient. Other drugs can be added if necessary. The goal of treatment is to make the patient as ambulatory and symptom-free as possible without causing supine hypertension.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Hypertension in women.

More women than men eventually develop hypertension in the United States due to their higher numbers and longer longevity. The white coat hypertension is also more common in women. Alcohol, obesity and oral contraceptives are important causes of rise in blood pressure among women. On the other hand, hormone replacement therapy may decrease cardiovascular mortality in the postmenopausal woman. Women with left ventricular hypertrophy are at a greater risk of death than men. Fibromuscular hyperplasia and primary aldosteronism are more common as causes of secondary hypertension in women. Nonpharmacologic therapy, such as weight reduction, exercise, salt and alcohol reduction, should always be tried prior to medical treatment of hypertension and are very useful adjunctive measures in controlling hypertension. ACE inhibitors and angiotensin receptor blockers are contraindicated in pregnancy and should be avoided in women with childbearing potential. Hypertension remains a major public health problem among black women. Although the antihypertensive drug therapy seems to benefit white women the least, proportionately more of them comply with their antihypertensive therapy. Hypertension is the most common chronic medical condition requiring visits to the physicians, as well as prescription medications, in the United States. The epidemiology, clinical course, response to treatment and ultimate outcome of essential hypertension may vary with gender. More women than men eventually develop hypertension in the US due to their higher numbers and longer longevity.

Antihypertensive Agents↗
PubMed1999

What is causing your patient's sexual dysfunction? Uncovering a connection with hypertension and antihypertensive therapy.

Arterial hypertension is associated with structural and functional alterations of the vessel walls. Because vascular endothelium plays a central role in the control of vascular tone, endothelial dysfunction can also cause certain types of erectile dysfunction. Erectile dysfunction is also a common side effect of certain drugs, including many antihypertensive agents. Physicians should be aware of potential sexual side effects of such drugs and take appropriate steps to alleviate persistent problems. Most important, physicians need to ask patients about sexual function and discuss the possibility of erectile dysfunction caused by antihypertensive therapy. Erectile dysfunction can be effectively treated in most patients, and many treatment options are available. Sildenafil therapy has revolutionized the management of this disorder, but this agent should be used with caution in certain patients taking nitrates.

Antihypertensive Agents↗
PubMed1999

Hyperhomocysteinemia: an additional cardiovascular risk factor.

Over the past few years, a substantial body of evidence has accumulated that indicates hyperhomocysteinemia as a significant risk factor for cardiovascular disease. Hyperhomocysteinemia arises from a lack of key enzymes or vitamins such as methylenetetrahydrofolate reductase, vitamin B6, and folate which are involved in homocysteine metabolism. Heavy coffee consumption is also known to elevate homocysteine levels. The adverse effects associated with hyperhomocysteinemia are extensive. It increases risk of myocardial infarction, cardiovascular-related morbidity and mortality, peripheral vascular disease, atherosclerosis, coronary heart disease, and cerebrovascular disease. Its seriousness as a risk factor has been equated to hypercholesterolemia and smoking, two leading causes for cardiovascular disease. It also has been shown to produce a multiplicative effect with these and other risk factors such as hypertension. Two major hypotheses have been proposed to explain how homocysteine induces its harmful effects. It can damage endothelial cells lining the vasculature, allowing plaque formation. Simultaneously, it interferes with the vasodilatory effect of endothelial derived nitric oxide. Also, homocysteine has been found to promote vascular smooth muscle cells hypertrophy. Both of these processes induce vessel occlusion. Maintaining a normal plasma level of homocysteine as a means to prevent cardiovascular disease appears promising. This is achieved through increased intake of folate and vitamin B6 through diet or supplementation. Despite the overwhelming evidence suggesting homocysteine as a significant risk factor, no long-term prospective studies have been completed to demonstrate that folate and vitamin B6 can prevent cardiovascular disease related morbidity and mortality in patients with hyperhomocysteinemia. Homocysteine is a key metabolite in amino acid synthesis. During the process of methylation, S-adenosylmethionine (Ado Met), derived from methionine, is converted to S-Adenosylhomocysteine (Figure 1). This product is quickly hydrolyzed to form homocysteine and adenosine. Homocysteine can undergo 1 of 3 reactions depending on the status of the organism. If cysteine levels are inadequate, homocysteine utilizes the coenzyme pyridoxal phosphate (vitamin B6) to condense with serine, forming the intermediate cystathionine. Subsequent reactions with cystathionine lead to the formation of cysteine. When methionine levels are low, homocysteine is remethylated in a reaction involving the coenzyme N5-methyltetrahydrofolate or betaine. Finally, when both amino acids are in adequate supply, homocysteine is cleaved by the enzyme homocysteine desulthydrase (cystathionase) to form a-ketobutyrate, ammonia, and H2S. Thus, homocysteine's physiological role is to assist in maintaining sulfur-amino acid homeostasis. Beyond these metabolic processes, homocysteine is beginning to be recognized as a significant risk factor for cardiovascular disease including atherosclerosis, coronary artery disease, cerebrovascular disease, and myocardial infarction.

Cardiovascular Diseases↗
PubMed1998

The costs versus the perceived benefits of an LCME institutional self-study.

PURPOSE: To calculate the costs versus the perceived benefits of an institutional self-study done to satisfy the requirements of the Liaison Committee on Medical Education's (LCME's) accreditation process. METHOD: From postcard questionnaires, the authors determined the hours spent over 18 months from 1994 to 1996 on the institutional self-study by 131 self-study committee members and 64 database compilers at the Medical College of Wisconsin. The committee members also rated the potential utility of the self-study process and the probability that the concerns identified by their subcommittees would be addressed. Administrative costs (self-study coordinating team's hours, supplies, and other expenses) were tracked using calendars and budget subaccount numbers. Personnel costs were calculated using salary data from the Association of American Medical Colleges and the College and Universities Personnel Administrators' survey. RESULTS: Supplies and equipment for the self-study cost $12,158, and the personnel costs, based on an 81% response rate, were estimated at $207,384, for a total of $219,542. The participants in the self-study rated the process as moderately useful, but believed that there was only a medium degree of probability that concerns they had identified would be addressed. CONCLUSION: Considering the costs of self-study, the process might be more useful if attention were focused less on identifying concerns and more on an institution's demonstrated ability to successfully respond to problems.

Computer-Assisted Instruction↗
PubMed1998

Stress and hypertension.

Stress can cause hypertension through repeated blood pressure elevations as well as by stimulation of the nervous system to produce large amounts of vasoconstricting hormones that increase blood pressure. Factors affecting blood pressure through stress include white coat hypertension, job strain, race, social environment, and emotional distress. Furthermore, when one risk factor is coupled with other stress producing factors, the effect on blood pressure is multiplied. Overall, studies show that stress does not directly cause hypertension, but can have an effect on its development. A variety of non-pharmacologic treatments to manage stress have been found effective in reducing blood pressure and development of hypertension, examples of which are meditation, acupressure, biofeedback and music therapy. Recent results from the National Health and Nutrition Examination Survey indicate that 50 million American adults have hypertension (defined to be a systolic blood pressure of greater than 139 mm Hg or a diastolic blood pressure of greater than 89 mm Hg). In 95% of these cases, the cause of hypertension is unknown and they are categorized as "essential" hypertension. Although a single cause may not be identified, the general consensus is that various factors contribute to blood pressure elevation in essential hypertension. In these days of 70 hour work weeks, pagers, fax machines, and endless committee meetings, stress has become a prevalent part of people's lives; therefore the effect of stress on blood pressure is of increasing relevance and importance. Although stress may not directly cause hypertension, it can lead to repeated blood pressure elevations, which eventually may lead to hypertension. In this article we explore how stress can cause hypertension and what can be done about it.

Adult↗
PubMed1997

Calcium channel blockers. Consensus amid controversy.

Although the calcium channel blockers have been used to treat hypertension for a number of years, they are now under close scrutiny because of disturbing findings regarding their safety. Drs Kochar and Qurashi sort out the controversies surrounding these widely used drugs and make recommendations based on current consensus.

Antihypertensive Agents↗
PubMed1997

Detection of hepatitis B surface antigen in whole blood by coupled particle light scattering (Copalis).

Coupled particle light scattering (Copalis) is a homogeneous immunoassay technology that permits simultaneous determination of multiple analytes in serum, plasma, or whole blood. Copalis differentiates monomeric latex microparticles from latex aggregates and cells on the basis of their unique light scatter properties. Copalis readily discriminates small (approximately 0.1 micron) differences in latex microparticle size. Therefore, multiple simultaneous assays are configured by the use of mixtures of different-size latex microparticles. The Copalis research immunoassay for hepatitis B surface antigen (HBsAg) is configured in a sandwich format where the extent of light scatter histogram broadening due to HBsAg-mediated binding of colloidal gold to latex provides the basis for antigen quantification. Simultaneous Copalis forward- and wide-angle light scatter measurements allow discrimination of latex microparticles from the cell components of whole blood. Consequently, direct detection of HBsAg in unprocessed whole-blood samples by Copalis is feasible.

Hematocrit↗
PubMed1996

Comparison of plasma lipid and lipoprotein profiles in hypertensive black versus white men. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.

An abnormal plasma lipid and lipoprotein profile is an independent and strong predictor of mortality and morbidity from coronary artery disease (CAD). We report on plasma lipid and lipoprotein profiles with respect to race, age, obesity, blood pressure (BP), smoking, and drinking history in 1,292 male veterans with a diastolic BP of 95 to 109 mm Hg while off antihypertensive medications. Blacks had 24% (p <0.001) lower triglycerides than whites. In contrast, the following parameters were higher in blacks than in whites by the indicated percentages: high-density lipoprotein (HDL) cholesterol, 16% (p <0.001); HDL2 cholesterol, 36% (p <0.001); apolipoprotein (Apo) A1, 8% (p <0.001); HDL/low-density lipoprotein (LDL), 18% (p = 0.018); HDL2/LDL, 36% (p = 0.031); HDL2/HDL3, 21% (p <0.001); and Apo A1/Apo B, 15% (p <0.001). Triglycerides were unchanged up to age 60, but were lower by 24% (p <0.001) in those aged > or = 70. Apo A1 levels were higher (p <0.001), whereas LDL cholesterol was lower (p <0.008) in moderate alcohol consumers versus abstainers. Triglycerides were higher (p <0.001), whereas HDL, HDL2 cholesterol, and Apo A1 were lower (p <0.001) with increasing obesity. Moderate alcohol consumption had a strong favorable effect on HDL, HDL2, and HDL3 cholesterol among subjects of normal weight, but this effect was diminished in obese subjects. Total and LDL cholesterol were higher by 6.4% (p = 0.001) and 9.4% (p <0.003), respectively, whereas HDL cholesterol remained unchanged in those with diastolic BP of 105 to 109 mm Hg versus those with diastolic BP of 95 to 99 mm Hg. We conclude that hypertensive black men have lipid and lipoprotein profiles indicative of less CAD risk than white men. Chronic moderate alcohol consumption correlates with a favorable plasma lipid and lipoprotein profile in normal, but not obese, men. Obesity is associated with an adverse plasma lipid and lipoprotein profile. Thus, race, alcohol intake, and obesity may be important modifiers of CAD in untreated hypertensive men.

Apolipoprotein A-I↗
PubMed1996

A medical school-based GME consortium in Milwaukee.

Consortia have been recommended as a local mechanism for allocating housestaff positions and overseeing graduate medical education (GME) training programs. They also could serve to simplify the execution of a national health care policy in the future. Such a consortium has existed in Milwaukee for the last 16 years. It involves 23 health care institutions affiliated with the Medical College of Wisconsin. Known as the Medical College of Wisconsin Affiliated Hospitals, Inc. (MCWAH), this consortium employs 749 housestaff, for whom it provides salary and benefits. It also ensures accreditation of all of its residency and fellowship programs and assists in providing direction and coordination for the member institutions. The authors describe the genesis and operation of the MCWAH in detail. The accomplishments of existing consortia, in Milwaukee and elsewhere, indicate that a GME consortium should enable its members to function effectively and efficiently in meeting the challenging GME training requirements of the future.

Career Choice↗
PubMed1996

The additive effects of smoking and hypertension. More reasons to help your patients kick the habit.

Although the link between cigarette smoking and its cardiovascular effects is well established, the mechanisms through which smoking raises blood pressure remain to be clarified. Possible mechanisms include nicotine-induced peripheral and central sympathetic nervous system stimulation, persisting levels of nicotine in blood because of incomplete metabolism, release of vasopressin, and chemoreceptor stimulation. Effects of nicotine on hemostasis, arterial rigidity, and vessel wall damage, together with detrimental effects on lipid metabolism, may contribute to an overall increased cardiovascular risk in smokers. Nonselective beta blockers are not as effective in smokers as they are in nonsmokers. Smoking cessation is a very important intervention in reducing cardiovascular risk in hypertensive patients. Physicians should counsel patients about smoking cessation at every visit. Use of the various smoking deterrents can help some patients quit.

Antihypertensive Agents↗
PubMed1995

Response to a second single antihypertensive agent used as monotherapy for hypertension after failure of the initial drug. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.

BACKGROUND: An important issue in clinical practice is how to treat patients whose blood pressure does not respond to the first antihypertensive drug selected. OBJECTIVE: To analyze the antihypertensive response of patients who had failed to achieve their diastolic blood pressure goal (< 90 mm Hg at the end of 8 to 12 weeks of titration) with one of six randomly allocated drugs or placebo to the random allocation of an alternate drug. METHODS: We initially randomized 1292 men with diastolic blood pressure of 95 to 109 mm Hg to treatment with hydrochlorothiazide, atenolol, captopril, clonidine hydrochloride, diltiazem hydrochloride (sustained release), prazosin hydrochloride, or placebo. Of 410 men in whom initial treatment failed, 352 qualified for randomization to the alternate drug. RESULTS: Of the 352 patients, 173 (49.1%) achieved their goal diastolic blood pressure, in 133 (37.8%) the alternate drug failed, and 46 (13.1%) left the study for various reasons. Overall response rates were as follows: diltiazem, 63%; clonidine, 59%; prazosin, 47%; hydrochlorothiazide, 46%; atenolol, 41%; and captopril, 37%. The best response rate for patients in whom hydrochlorothiazide failed was achieved with diltiazem (70%); after atenolol failure, clonidine (86%); after captopril failure, prazosin (54%); after clonidine failure, diltiazem (100%); after diltiazem failure, captopril (67%); and after prazosin failure, clonidine (53%). The combined response rate for patients initially randomized to an active treatment was 76.0%, which is similar to that achieved by the combination of two drugs in previous studies. CONCLUSIONS: We conclude that sequential single-drug therapy is a rational approach for treatment of hypertension in patients in whom initial drug therapy has failed.

Adult↗
PubMed1994

Hypertension in the diabetic patient. Controlling its harmful effects.

When diabetes and hypertension occur in the same patient, good control of both is needed to slow the progression of atherosclerosis and diabetic nephropathy. Antihypertensive agents must be selected with caution, as they may have side effects that are detrimental to diabetic patients. Drs Kochar and Kalluru review the types of hypertension that are common with diabetes and discuss both lifestyle modifications and pharmacologic therapy.

Diabetes Complications↗
PubMed1994

Alcohol and hypertension.

The link between alcohol and hypertension is well established, yet the mechanism through which alcohol raises blood pressure remains elusive. Possible mechanisms include an imbalance of the central nervous system, impairment of the baroreceptors, an increase of sympathetic activity, stimulation of the renin-angiotensin-aldosterone system, an increase in cortisol levels, an increase of intracellular calcium levels with a subsequent increase in vascular reactivity, stimulation of the endothelium to release endothelin or inhibition of endothelium-dependent nitric oxide production, and chronic subclinical withdrawal. For control of hypertension, cessation or at least reduction of alcohol intake is the first step. Pharmacologic treatment should be withheld until after 2 to 4 weeks of abstinence from alcohol. Alcoholism can result in autonomic neuropathy and cardiomyopathy that can lead to a fall in blood pressure. We believe that angiotensin-converting enzyme inhibitors and calcium channel blockers may be the most appropriate pharmacologic treatment.

Alcohol Drinking↗
PubMed1994

Sequential monotherapy of hypertension.

In most cases, the antihypertensive therapy for an individual patient is selected through a process of trial and error. This study determined if, by treating each hypertensive patient sequentially, with six antihypertensive drugs, one from each of the major classes, one could decide on the best possible drug for control of hypertension. In a randomized open-label crossover study, 19 patients (16 male and 3 female), 28-70 years of age with a sitting diastolic blood pressure of 95-110 mm Hg were given atenolol, captopril, clonidine, indapamide, prazosin, and verapamil in a sequential manner. Each drug was started at the minimum recommended or lower dose and titrated upwards every 2 weeks, if well tolerated, until blood pressure was controlled (diastolic BP < 90 mm Hg). If blood pressure was controlled, the drug was continued for another 2 weeks. A washout period of at least 2 weeks was allowed between drugs. Both systolic and diastolic blood pressures were reduced significantly with all of the six drugs. In 18 of the 19 patients, blood pressure was controlled with at least one of six drugs, frequently with the lowest dose. The authors conclude that if hypertension is not controlled with the lowest recommended dose of a drug, other antihypertensive drugs should be tried sequentially rather than increasing the dose or adding a second drug.

Adult↗