Search PubMed⌕ Search

Biomedical subjects

E Grossman

Publications and source records attributed to E Grossman.

At least 37 records · Page 2Linked to original sources
PubMed2001

The significance of hypertensive response to exercise as a predictor of hypertension and cardiovascular disease.

Several studies have shown that exaggerated blood pressure (BP) response to exercise can predict the development of hypertension and target organ damage, but others did not. The aim of this study was to evaluate the relationship between exaggerated BP response to exercise (ExBPR) and the development of hypertension or cardiovascular disease. We reviewed the charts of male subjects who, during the years 1991-1994, had a routine check up that included an exercise stress-test. For each subject, the following parameters were noted: age; body mass index (BMI); history of diabetes; cigarette smoking; family history of ischaemic heart disease and lipid profile. BP and heart rate at rest and during exercise were recorded as well. ExBPR was defined whenever peak exercise systolic BP or diastolic BP was over 200 mm Hg or 100 mm Hg respectively. We identified 73 males who exhibited ExBPR and matched them with a control group of 117 subjects with similar age who had a normal BP response. The mean age of the studied group was 42.6 years and the average follow-up was 5.7 years. Baseline characteristics were similar in both groups. During the follow-up we observed hypertension among 22% in those with ExBPR in contrast to 2.6% in the control group (P < 0.0001). In addition, more subjects of the ExBPR group required cardiovascular medications than of those in the control group (19.2% vs 4.3%, P = 0.0008). Thus, it seems that ExBPR predicts the development of hypertension and cardiovascular diseases. We therefore suggest that subjects with ExBPR should be followed more closely and be instructed for lifestyle modifications which may delay the development of such diseases.

Adult↗
PubMed2001

Long-term diuretic therapy in patients with coronary disease: increased colon cancer-related mortality over a 5-year follow-up.

OBJECTIVES: Recent studies have suggested that long-term diuretic therapy may be associated with increased risk of renal cell carcinoma. This carcinoma is not a common malignancy, but it shares risk factors with the considerably more widespread colon cancer (CC). However, there are no data whether or not a relationship between long-term diuretic therapy and CC mortality exists. In this study we tested the hypothesis that long-term diuretic therapy may be associated with increased CC mortality over a 5.6-year follow-up period. SUBJECTS AND METHODS: The study sample comprised 14 166 patients aged 45 to 74 years with a previous myocardial infarction and/or stable anginal syndrome, screened for participation in the bezafibrate infarction prevention (BIP) study. There were 2153 patients receiving diuretics and 12 013 patients receiving no diuretics. RESULTS: During the follow-up 139 (6.5%) new cases of cancer were diagnosed in the diuretic-treated group compared with 622 (5.2%) in the group receiving no diuretics (P = 0.02). Colon cancer mortality was significantly higher in the diuretic-treated patients (0.1 vs 0.5%, P = 0.001), whereas mortality differences for other cancer types were not documented. Multivariate analysis identified diuretics as an independent predictor of increased colon cancer incidence and colon cancer mortality with a hazard ratio (HR) of 2.0 (95% CI 1.2-3.2) for colon cancer incidence and 3.7 (95% CI 1.7-8.3) for mortality. However, the association between diuretic therapy and higher incidence of colon cancer was observed only among non-users of aspirin. A relatively lower colon cancer incidence was observed in the furosemide subgroup, and higher in the small combined amiloride/hydrochlorthiazide subgroup (HR 3.15, 95% CI 1.15-8.65). CONCLUSION: Long-term exposure to diuretic therapy may be associated with an increased colon cancer-related mortality.

Aged↗
PubMed2001

Prevalence and determinants of erectile dysfunction in hemodialysis patients.

BACKGROUND: The prevalence of erectile dysfunction (ED) among patients with end-stage renal disease (ESRD) is not known. METHODS: A cross-sectional study was conducted to determine the prevalence of ED among a community-based hemodialysis (HD) population using a two-stage cluster random sampling design. The presence and severity of ED were assessed among 302 ESRD patients using the self-administered International Index of Erectile Function-5 (IIEF-5). Logistic regression was used to examine and test associations between ED and other medical conditions. RESULTS: The prevalence of any level of ED was 82% (95% CI, 76 to 87%) for all HD subjects. The prevalence of severe ED was 45% (CI, 36 to 55%). Subjects younger than 50 years had a prevalence of ED of 63% (CI, 53 to 71%), while in subjects 50 years or older, it was 90% (CI, 84 to 94%). A multivariable analysis demonstrated increasing age (50 to 59, OR = 2.04, 95% CI, 1.3 to 3.1; 60 to 69, OR = 5.5, 95% CI, 1.9 to 15.6) and diabetes (OR = 2.0, 95% CI, 1.2 to 3.3) to be independently associated with the presence of any level of ED. However, neither the subjects' age nor history of diabetes predicted the severity of ED among subjects with ED. The use of angiotensin-converting enzyme inhibitors (ACEIs) was inversely associated with ED (OR = 0.41, 95% CI, 0.17 to 0.98). Poor functional status (Karnofsky score or the Index of Physical Impairment) was not associated with ED. CONCLUSIONS: ED is extremely prevalent among HD patients. Increasing age, diabetes, and nonuse of ACEIs were associated with higher prevalence of ED. The high prevalence of ED was seen even among patients with good functional status.

Adult↗
PubMed2001

Antihypertensive therapy and the risk of malignancies.

AIMS: To assess the relationship between antihypertensive therapy and malignancy. METHODS AND RESULTS: A MEDLINE search for English-language articles published between January 1966 and August 1999 identified 29 prospective studies that reported cancer incidence or mortality and 28 case-control studies that reported specific drug use in cancer patients and controls. The association between rauwolfia derivatives and breast cancer was analysed in 5852 cases and 9776 controls, yielding an odds ratio (OR) of 1.25 (95% CI, 1.09-1.44). The association between diuretics and renal cell carcinoma was analysed in 4389 cases and 6566 controls, yielding a pooled OR of 1.54 (95% CI, 1.41-1.68). The association between atenolol and cancer death was analysed pooling three randomized controlled studies, including 1879 treated patients and 3078 non-treated patients, yielding a pooled OR of 1.36 (95% CI, 1.02-1.82); however, data from non-randomized studies did not confirm the latter. The association between calcium antagonists and malignancy was analysed pooling five randomized controlled studies, including 5451 treated patients and 5207 untreated ones, yielding a pooled OR of 0.78 (CI, 0.60-1.00). A meta-analysis of an additional five longitudinal studies, including 9087 treated patients and 15 559 non-treated patients, yielded a pooled OR of 1.04 (CI, 0.91-1.19). The association between ACE inhibitors and malignancy was analysed pooling two randomized controlled trials involving 1585 treated patients and 1567 non-treated patients, yielding a pooled OR of 1.57 (95% CI, 0.97-2.57); however, non-randomized studies showed no association or a decreased risk for malignancy with ACE inhibitors. CONCLUSIONS: With the exception of diuretics and renal cell carcinoma, the association between antihypertensive drugs and malignancy was either low grade (rauwolfia), uncertain (atenolol), absent (ACE inhibitors), or absent with a yet to be investigated inverse association (calcium antagonists). Ongoing long-term prospective studies with cardiovascular drugs should carefully monitor the risk of malignancy.

Adrenergic beta-Antagonists↗
PubMed2001

Reproducibility of exaggerated blood pressure response to exercise in healthy patients.

BACKGROUND: An exaggerated blood pressure response (ExBPR) to exercise has been shown to be predictive of future hypertension and left ventricular hypertrophy. The aim of this study was to test the reproducibility over time of ExBPR and to better characterize patients who consistently respond in this manner. METHODS: During periodical health examination, patients underwent routine treadmill exercise testing. ExBPR was said to be present if systolic blood pressure and/or diastolic blood pressure at peak exercise exceeded 200 mm Hg and 100 mm Hg, respectively. Over the past 25 years, 117 healthy patients with ExBPR performed 2 to 7 consecutive treadmill exercise tests. According to subsequent ExBPR, these patients were divided into a concordant group-those who had at least two-thirds repetitions of the ExBPR-and a discordant group-those who had less than two-thirds repetitions. For comparison, we identified patients who did not have ExBPR (control group). RESULTS: Of the 117 patients who had ExBPR, only 18 (15.4%) were in the concordant group in subsequent tests. No clinical features were found to characterize patients in the concordant group. In the two study groups, the variability of blood pressure measurements during stress was significantly greater than in the control group. Also, systolic blood pressure measurements at rest and after 3 minutes of recovery were significantly lower in the control group. CONCLUSIONS: ExBPR to exercise is rarely reproducible, and there are no clinical findings characterizing those who consistently respond in this manner. Thus the prognostic importance of blood pressure response to exercise should be reconsidered.

Adult↗
PubMed2001

Coronary benefits of calcium antagonist therapy for patients with hypertension.

Calcium antagonists effective in lowering blood pressure are a heterogeneous group including three main classes: phenylalkylamines, benzothiazepines and dihydropyridines. Dihydropyridines have a dual mode of action upon the endothelium contributing to their beneficial antihypertensive effects: (1) direct relaxation by inhibition of smooth muscle L-type calcium current, and (2) indirect relaxation through release of nitric oxide from the vascular endothelium. Calcium antagonists may affect many calcium-dependent events in the formation of atherosclerosis such as the localized accumulation of collagen, elastin, and calcium together with monocyte infiltration and smooth muscle proliferation and migration. In the INSIGHT calcification study, the overall treatment effect of nifedipine demonstrated significant inhibition of coronary calcium progression over a three-year period. Calcium antagonists improve symptoms and reduce ischemia in hypertensive patients with ischemic heart disease. Although in placebo-controlled trials calcium antagonists demonstrated a significant reduction in cardiovascular morbidity and mortality, they may be less effective than other types of antihypertensive drugs in preventing ischemic heart disease.

Angina Pectoris↗
PubMed2001

Angiotensin II-induced apoptosis in rat cardiomyocyte culture: a possible role of AT1 and AT2 receptors.

OBJECTIVES: To investigate the mechanism of angiotensin II-induced apoptosis in cultured cardiomyocytes by determining which receptor subtype is involved, and what is the relationship between intracellular Ca2+ changes and apoptosis. DESIGN AND METHODS: Neonatal rat cardiomyocytes were pretreated with either the AT1 antagonist irbesartan or the AT2 antagonist PD123319 before exposure to angiotensin II. Apoptosis was evaluated using morphological technique, staining nuclei by Feulgen and Hoechst methods followed by image analysis and by in situ terminal deoxynucleotidyl transferase nick-end (TUNEL) labelling. TUNEL-positive cardiocytes were distinguished from other cells by double staining with alpha-sarcomeric actin. Intracellular Ca2+ changes were assessed by indo-1 fluorescence microscopy, and the effect of Ca2+ on angiotensin II-induced apoptosis was tested using the calcium channel blocker verapamil. RESULTS: Exposure to angiotensin II (10 nmol/l) resulted in cell replication and a three-fold increase in programmed cell death (P < 0.05). Pretreatment with either irbesartan (an AT1receptor antagonist, 100 nmol/l) or PD123319 (an AT2 receptor antagonist, 1 micromol/l) prevented the angiotensin II-induced apoptosis, indicating the presence of both AT1 and AT2receptors on cardiomyocytes. Exposure of myocytes to angiotensin II caused an immediate and dose-dependent increase in the concentration of intracellular free Ca2+ that lasted 40-60 s. The effect was sustained in a Ca2+ free medium. Pretreatment of cells with irbesartan (100 nmol/l) and PD123319 (10 micromol/l) blocked Ca2+ elevation. Pretreatment with verapamil (10 micromol/l) prevented angiotensin II-induced apoptosis. CONCLUSIONS: Angiotensin II-induced apoptosis in rat cardiomyocytes is mediated through activation of both AT1 and AT2 receptors. The apoptotic mechanism is not related to the immediate angiotensin II-induced Ca2+ rise from intracellular stores. However, it is accompanied by cardiomyocyte proliferation and requires Ca2+ influx through L-type channel activity.

Angiotensin II↗
PubMed2000

High blood pressure and diabetes mellitus: are all antihypertensive drugs created equal?

OBJECTIVE: To analyze the available data to assess the benefits of antihypertensive therapy in hypertensive patients with diabetes mellitus. METHODS: A MEDLINE search of English-language articles published until June 1999 was undertaken with the use of the terms diabetes mellitus, hypertension or blood pressure, and therapy. Pertinent articles cited in the identified reports were also reviewed. Included were only prospective randomized studies of more than 12 months' duration that evaluated the effect of drug treatment on morbidity and mortality in diabetic hypertensive patients. We estimated the risk associated with combination of diabetes mellitus and hypertension and the effect of treatment on morbidity and mortality. RESULTS: The coexistence of diabetes mellitus doubled the risk of cardiovascular events, cardiovascular mortality, and total mortality in hypertensive patients (approximate relative risk of 1.73-2.77 for cardiovascular events, 2.25-3.66 for cardiovascular mortality, and 1.73-2.18 for total mortality). Intensive blood pressure control to levels lower than 130/85 mm Hg was beneficial in diabetic hypertensive patients. All 4 drug classes-diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, and calcium antagonists-were effective in reducing cardiovascular events in diabetic hypertensive patients. In elderly diabetic patients with isolated systolic hypertension, calcium antagonists reduced the rate of cardiac end points by 63%, stroke by 73%, and total mortality by 55%. In more than 60% of diabetic hypertensive patients, combination therapy was required to control blood pressure. CONCLUSIONS: Intensive control of blood pressure reduced cardiovascular morbidity and mortality in diabetic patients regardless of whether low-dose diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, or calcium antagonists were used as a first-line treatment. A combination of more than 1 drug is frequently required to control blood pressure and may be more beneficial than monotherapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

[Prolonged neuromuscular damage following corticosteroids and muscle relaxants].

Many patients mechanically ventilated for acute respiratory failure, are treated with medication that includes a combination of cortico-steroids and non-depolarizing neuromuscular-blocking agents (NNBa). A third of them can be expected to develop delayed neuromuscular damage, which may be severe and prolonged. We describe a 50-year-old man who suffered from acute myeloid leukemia and was ventilated due to pneumonia. He was treated with pancuronium and cortico-steroids, and during recovery suffered quadriparesis that lasted several months. Typically this damage is purely motor and is accompanied by absent tendon-reflexes, sometimes with elevated creatine-kinase. Muscle biopsy usually shows deletion and degeneration of thick myosin filaments. The phenomenon is related to the duration of NNBa treatment, and probably results from an adverse synergistic effect on muscle tissue of the cortico-steroids and cortico-steroid-like NNBa given the immobilized patient. Awareness of this adverse effect of steroids and pancuronium, the use of passive mobilization, shortening the use of NNBa and early rehabilitation would minimize disability due to this phenomenon.

Adrenal Cortex Hormones↗
PubMed2000

Effects of losartan and candesartan monotherapy and losartan/hydrochlorothiazide combination therapy in patients with mild to moderate hypertension. Losartan Trial Investigators.

OBJECTIVE: The goal of this multicenter, double-blind, randomized, parallel-group study was to compare the effects of losartan potassium (hereafter referred to as losartan), candesartan cilexitil (hereafter referred to as candesartan), and losartan/hydrochlorothiazide (HCTZ) in patients with mild to moderate hypertension (sitting diastolic blood pressure [SiDBP] 95-115 mm Hg). METHODS: A total of 1161 patients were randomized in a 2:2:1 ratio to 12 weeks of treatment with losartan 50 mg QD, possibly titrated to 100 mg QD (n = 461); candesartan 8 mg QD, possibly titrated to 16 mg QD (n = 468); or losartan 50 mg QD, possibly titrated to losartan 50 mg plus HCTZ 12.5 mg QD (n = 232). At 6 weeks, the regimens of patients not reaching a goal SiDBP <90 mm Hg were titrated as described, whereas patients achieving this goal continued with low-dose monotherapy. The single primary end point at 12 weeks tested the equivalence of the 2 monotherapy regimens, predefined as a maximum between-treatment difference in the mean change from baseline trough SiDBP of 2.5 mm Hg. RESULTS: At 12 weeks, changes in SiDBP/sitting systolic blood pressure (SiSBP) of -12.4/-14.4 mm Hg with losartan 50 mg/100 mg and -13.1/-15.8 mm Hg with candesartan 8 mg/16 mg demonstrated equivalence between the 2 monotherapy regimens (95% CI for difference in SiDBP, -1.6 to 0.2). At 12 weeks, the losartan 50 mg/50 mg plus HCTZ 12.5 mg regimen had reduced SiDBP/SiSBP significantly more (-14.3/-18.0 mm Hg) than either the candesartan 8 mg/16 mg (SiDBP, P = 0.045; SiSBP, P = 0.017) or losartan 50 mg/100 mg regimen (SiDBP and SiSBP, P = 0.001). During the last 6 weeks, patients whose regimen had been titrated to losartan 50 mg plus HCTZ 12.5 mg (n = 114) showed a greater reduction in SiDBP/SiSBP (-14.5/ -18.7 mm Hg) than did those whose regimen had been titrated to either losartan 100 mg (-10.5/-12.3 mm Hg; n = 211) or candesartan 16 mg (-11.5/-13.2 mm Hg; n = 206), representing a clinically meaningful > or = 2.5-mm Hg) difference. All 3 treatments were well tolerated, with few patients experiencing drug-related adverse events (6.9% losartan 50 mg/100 mg, 7.5% candesartan 8 mg/16 mg, 3.0% losartan 50 mg/ 50 mg plus HCTZ 12.5 mg). Candesartan 8 mg/16 mg increased serum uric acid levels (0.13 mg/dL; 95% CI, 0.04 to 0.23), whereas losartan 50 mg/100 mg decreased them (-0.14 mg/dL; 95% CI, -0.24 to -0.04), and losartan 50 mg/50 mg plus HCTZ 12.5 mg left them unchanged (0.06 mg/dL; 95% CI, -0.07 to 0.20). CONCLUSIONS: Losartan 50 mg/100 mg and candesartan 8 mg/16 mg were comparable treatments in terms of blood pressure reduction. After titration, losartan 50 mg plus HCTZ 12.5 mg was superior to either candesartan 16 mg or losartan 100 mg in reducing hypertension. Losartan, but not candesartan, lowered serum uric acid levels and attenuated the expected increase in uric acid levels with HCTZ 12.5 mg.

Adult↗
PubMed2000

Intermediate but not low doses of aspirin can suppress angiotensin-converting enzyme inhibitor-induced cough.

This self-matched control study aimed to compare the efficiency of two different regimens of active treatment: aspirin in low (100 mg daily) versus intermediate (500 mg daily) doses in abolishing angiotensin-converting enzyme inhibitor (ACEI)-induced cough. A dry bothersome cough is the most common adverse class effect of all angiotensin-converting enzyme inhibitors. Prostaglandins (PG) have been pinpointed as playing a leading role in the genesis of ACEI-associated cough. The role of different doses of the most commonly used PG inhibitor-aspirin-in ACEI cough modification was not yet elucidated. Of 350 consecutive ACEI-treated patients, we identified 34 (9.7%) nonsmoking ACEI-related coughers. Patients with lung disease, nonsteroidal anti-inflammatory drug (NSAID) treatment, and those who did not agree to participate in the study were excluded. In the remaining 14 ACEI coughers (eight men, six women; mean age, 63 +/- 11 years), the treatment was discontinued; the dry cough completely disappeared, but returned in all patients within 1 week after ACEI reintroduction. At the end of the rechallenge period, patients started a low dose of aspirin for 1 week, switching thereafter to the intermediate dose of aspirin for an additional week. On each visit the cough severity (CS, 0-4) and frequency (CF, 0-10) scores were registered. Low doses of aspirin were ineffective in suppressing ACEI-induced cough, whereas intermediate doses completely abolished cough in five patients and reduced coughing in all but one patient; CS and CF decreased, respectively, from 2.5 +/- 1.0 to 0.9 +/- 1.1, P < .002 and from 6.6 +/- 2.4 to 2.4 +/- 1.1, P < .0002. Overall, intermediate doses of aspirin beneficially modified cough scores in 13 (93%) patients, enabling nine (64%) to continue ACEI treatment. Aspirin did not influence blood pressure control either in hypertensives or in postinfarction patients. We conclude that intermediate but not low doses of aspirin probably can suppress ACEI-induced cough. These findings propose a new alternative therapeutic approach for patients with ACEI-related cough, especially those in whom ACEI treatment seems to be essential.

Aged↗
PubMed2000

Marked weight reduction lowers resting and exercise blood pressure in morbidly obese subjects.

Obesity and high blood pressure (BP) often coexist. Weight reduction lowers resting BP but its effect on BP during exercise (a predictor of target organ damage) has not been evaluated. Blood pressure was measured at rest and during cycling, before and after weight reduction induced by gastric restriction. Nineteen subjects (4 male), 41 +/-2 (SEM) years of age and body mass index (BMI) of 43 +/- 0.9 kg/m2, were studied. On each occasion BP was measured at rest, at a steady state of 0 and 25 watts, at peak exercise and 1 min into recovery. Body weight was reduced by 28% +/- 6% and BMI decreased from 43.3 +/- 0.9 to 31.5 +/- 0.7 kg/m2 (P < .01). Both BP and heart rate, at rest and at all exercise intensities, were significantly lower after weight reduction. Resting BP decreased from 133 +/-4/87 +/- 3 mm Hg to 115 +/- 4/77 +/- 2 mm Hg (P < .001), and BP at peak exercise decreased from 181 +/- 8/98 +/- 4 to 162 +/- 6/83 +/- 5 mm Hg (P < .001). The change in resting systolic BP did not correlate with the change in body weight or with the change in heart rate, but it correlated with the baseline systolic BP (R = 0.61; P < .005). It is concluded that marked weight reduction reduces BP at rest and at all exercise intensities. Gastroplasty should be considered as an option in morbidly obese hypertensive patients who are not well controlled with conventional treatment, and who fail to lose or to maintain a reduced weight by calorie restriction alone.

Adult↗