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M Jonas

Publications and source records attributed to M Jonas.

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

Fas (CD95) induces alveolar epithelial cell apoptosis in vivo: implications for acute pulmonary inflammation.

Activation of the Fas/FasL system induces apoptosis of susceptible cells, but may also lead to nuclear factor kappaB activation. Our goal was to determine whether local Fas activation produces acute lung injury by inducing alveolar epithelial cell apoptosis and by generating local inflammatory responses. Normal mice (C57BL/6) and mice deficient in Fas (lpr) were treated by intranasal instillation of the Fas-activating monoclonal antibody (mAb) Jo2 or an irrelevant control mAb, and studied 6 or 24 hours later using bronchoalveolar lavage (BAL), histopathology, DNA nick-end-labeling assays, and electron microscopy. Normal mice treated with mAb Jo2 had significant increases in BAL protein at 6 hours, and BAL neutrophils at 24 hours, as compared to lpr mice and to mice treated with the irrelevant mAb. Neutrophil recruitment was preceded by increased mRNA expression for tumor necrosis factor-alpha, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-2, macrophage chemotactic protein-1, and interleukin-6, but not interferon-gamma, transforming growth factor-ss, RANTES, eotaxin, or IP-10. Lung sections from Jo2-treated normal mice showed neutrophilic infiltrates, alveolar septal thickening, hemorrhage, and terminal dUTP nick-end-labeling-positive cells in the alveolar septae and airspaces. Type II pneumocyte apoptosis was confirmed by electron microscopy. Fas activation in vivo results in acute alveolar epithelial injury and lung inflammation, and may be important in the pathogenesis of acute lung injury.

Acute Disease↗
PubMed2001

Anal Fissure.

Anal fissure is a common condition, and although most are short-lived and heal spontaneously, those that persist and require intervention cause considerable morbidity in an otherwise healthy young population. Traditionally, lateral internal sphincterotomy was the gold standard treatment for chronic fissures, but this procedure is associated with a risk of incontinence to some degree in 30% of patients. The discovery of pharmacologic agents that effectively cause a chemical sphincterotomy and heal most fissures has led to approximately two thirds of patients avoiding surgery. Topical 0.2% GTN ointment probably is the most widely used first-line treatment. Other drugs currently under investigation may offer effective treatment with fewer side effects. Another advantage of these novel treatments is that by acting through different pathways, they may be effective in the 30% of cases in which GTN fails, the risks associated with surgery may be avoided. Studies of botulinum toxin injection into the anal sphincter have reported excellent healing rates, although the procedure is more invasive, and patients may find it uncomfortable and less tolerable. Chemical sphincterotomy is particularly suitable in patients with associated inflammatory bowel disease, in whom sphincterotomy for anal fissure generally is contraindicated. When pharmacologic therapy fails or fissures recur frequently and patients have raised resting anal pressure, lateral internal sphincterotomy is the surgical treatment of choice. The results are satisfactory when patients are selected carefully and the incision is limited to the length of the fissure. When chemical sphincterotomy fails and resting anal pressures are not elevated, as is commonly the case with patients developing fissures postpartum, an advancement flap should be considered.

Anal Canal↗
PubMed2001

Sulfonylureas are not associated with increased mortality in diabetics treated with thrombolysis for acute myocardial infarction.

BACKGROUND: Sulfonylurea compounds may impair ischemic preconditioning and endogenous fibrinolysis. Increased mortality has been reported in diabetics receiving these drugs prior to admission for acute myocardial infarction when treated by direct angioplasty. Although thrombolytics are currently employed far more frequently than direct angioplasty the effect of sulfonylureas on mortality in the setting of thrombolysis has not been previously addressed. METHODS: Two hundred forty five diabetics treated with either accelerated t-PA or streptokinase in a national, multi-center, randomized comparison of argatroban vs. heparin (n=1200) were grouped by anti-diabetic treatment prior to hospitalization, and their outcomes were compared by retrospective analysis. RESULTS: Baseline characteristics were similar in all groups (sulfonylureas: n=121, oral medications other than sulfonylureas: n=17, insulin: n=28, diet alone: n=79). Sulfonylurea use was not associated with increased mortality or adverse event rates. By logistic regression analysis with diet treatment as reference, only prior insulin use was associated with higher risk for mortality at 30 days and 1 year (odds ratios 4.5 and 5.22, respectively, p<0.05). CONCLUSIONS: Sulfonylureas use prior to admission is not associated with adverse outcomes in diabetics treated with thrombolytics for myocardial infarction. Since direct angioplasty may increase mortality in patients taking these drugs, a randomized trial is needed to specifically compare different strategies of acute reperfusion in diabetics.Abbreviated abstract. Increased mortality has been reported in diabetics using sulfonylureas when treated for myocardial infarction by direct angioplasty. No study has specifically addressed the effect of these drugs on outcomes in the setting of thrombolysis. In a retrospective analysis of 245 diabetics treated with thrombolysis in a randomized comparison of argatroban vs. heparin, outcomes were compared in relation to anti-diabetic therapy prior to admission. Sulfonylurea use did not adversely affect prognosis, which was worst among diabetics previously treated with insulin. In conclusion, sulfonylureas do not worsen outcomes of diabetics treated with current thrombolytic regimens in comparison with other anti-diabetic treatments.

Aged↗
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

Systemic levels of glyceryl trinitrate following topical application to the anoderm do not correlate with the measured reduction in anal pressure.

BACKGROUND: Topical 0.2 per cent glyceryl trinitrate (GTN) lowers resting anal pressure (RAP) and heals two-thirds of chronic anal fissures. Over 50 per cent of patients experience headache, presumably through systemic absorption, but the pharmacokinetics of GTN ointment are unknown. This study evaluated the systemic absorption profile of GTN, and correlation between plasma GTN levels, RAP, haemodynamic variables and side-effects. METHODS: Thirty healthy volunteers were recruited with local medical school ethics committee approval. Continuous static anal manometry was performed for 10 min before and 2 h after application of 0.2 per cent GTN (0.5 g) to the anoderm. Blood samples were taken from an intravenous cannula, and pulse and blood pressure were measured before application of GTN, and 10, 20, 30, 40, 50, 60, 90, 120 and 180 min thereafter. Details of side-effects were recorded. RESULTS: GTN was detected in the plasma 10 min to 3 h after topical application. RAP was significantly reduced after 10 min, but had returned to pretreatment values by 120 min. Pulse was statistically unchanged during the study; systolic blood pressure was significantly lower 20-90 min after GTN application, and diastolic pressure was decreased throughout the study. Headaches were experienced by 14 of 30 volunteers after a median (range) of 41 (4-120) min, persisting for 74 (30-176) min, with an intensity score of 19 (5-30) mm represented on a 100-mm linear visual analogue scale. There was no correlation between plasma GTN concentration, RAP, and the onset, duration or intensity of headaches. CONCLUSION: Topical GTN acts locally on the internal anal sphincter; systemic levels do not contribute significantly to the reduction in RAP. There is marked interindividual variation in plasma GTN levels, and no correlation with haemodynamic variables and side-effects.

Absorption↗
PubMed2001

Transcytosis of gastrointestinal epithelial cells by Escherichia coli K1.

Escherichia coli K1 is an important neonatal pathogen that is usually transferred from maternal to infant gastrointestinal tract at the time of parturition. Approximately 20% of neonates are colonized, and a proportion of colonized infants goes on to have systemic infection. Entry into the bloodstream from the gastrointestinal tract is hypothesized to occur via epithelial cell invasion. Invasion of multiple epithelial cell lines was studied using gentamicin protection assays and transcytosis of polarized monolayers. Electron microscopy was used to confirm cellular invasion. Cell lines used include two human gastrointestinal lines, Caco-2 and T84; a human respiratory cell line, A549; a human laryngeal cell line, HEp-2; and a canine kidney cell line, MDCK. A virulent E. coli K1 strain, RS218, readily invaded HEp-2, A549, and T84 cell lines in gentamicin protection assays, but was less invasive into MDCK and Caco-2 cells. RS218 also demonstrated transcytosis of both T84 and Caco-2 cells. Four clinical isolates of E. coli K1 demonstrated levels of transcytosis of T84 cells similar to RS218. Caco-2 invasiveness correlated with length of time in tissue culture with maximum invasiveness demonstrated at 11 d in culture, when cells were polarized and differentiated.

Animals↗
PubMed2000

Clinical profile and long-term prognosis of women < or = 50 years of age referred for coronary angiography for evaluation of chest pain.

A significant lack of information exists regarding risk factors, preventive strategies, diagnostic testing, and treatment of women with coronary artery disease (CAD), especially in the young age group. We studied the clinical profile, angiographic results, and long-term follow-up of 135 women aged < or =50 years referred for coronary angiography because of chest pain. The most prominent risk factor was hyperlipidemia (60%), followed by a family history of coronary disease (44%), systemic hypertension (40%), cigarette smoking (31%), postmenopausal state (23%), and diabetes mellitus (21%). Angiographically significant CAD was demonstrated in 79 of 135 patients (58%), most of whom (61%) had 1-vessel CAD. Women with compared to those without significant CAD had a higher prevalence of hyperlipidemia (71% vs 45%; p = 0.002) and of the post-menopausal state (30% vs 16%; p = 0.028). There was no difference in the incidence of positive noninvasive evaluation (ergometry or thallium scan) before catheterization between women with or without significant coronary lesions. At a follow-up period of 2 to 7 years, 3 women had acute myocardial infarction, all of whom demonstrated coronary lesions on prior angiography. No difference was found regarding the recurrence of chest pain on follow-up between women with or without significant CAD. Mortality and congestive heart failure were observed more frequently in women with CAD (6% vs 0%; p = 0.0516 and 12% vs 2%; p = 0.047, respectively).

Adult↗
PubMed2000

Myelokathexis, a congenital disorder of severe neutropenia characterized by accelerated apoptosis and defective expression of bcl-x in neutrophil precursors.

Myelokathexis is a congenital disorder that causes severe chronic leukopenia and neutropenia. Characteristic findings include degenerative changes and hypersegmentation of mature neutrophils and hyperplasia of bone marrow myeloid cells. The associated neutropenia can be partially corrected by treatment with granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF). These features led us to propose that accelerated apoptosis of neutrophil precursors might account for the neutropenic phenotype. Blood and bone marrow aspirates were obtained from 4 patients (2 unrelated families) with myelokathexis before G-CSF therapy and from 2 of the affected persons after G-CSF therapy (1 microg/kg per day subcutaneously for 3 weeks). Bone marrow was fractionated using immunomagnetic bead cell sorting into CD34(+), CD33(+)/CD34(-), and CD15(+)/CD34(-)/CD33(- )cell populations. Examination of these cells by flow cytometry and electron microscopy revealed abundant apoptosis in the CD15(+) neutrophil precursor population, characterized by enhanced annexin-V binding, extensive membrane blebbing, condensation of heterochromatin, and cell fragmentation. Colony-forming assays demonstrated significant reduction in a proportion of bone marrow myeloid-committed progenitor cells. Immunohistochemical analysis revealed a selective decrease in bcl-x, but not bcl-2, expression in the CD15(+)/CD34(-)/CD33(-)cell population compared with similar subpopulations of control bone marrow-derived myeloid precursors. After G-CSF therapy, apoptotic features of patients' bone marrow cells were substantially reduced, and the absolute neutrophil counts (ANC) and expression of bcl-x in CD15(+)/CD34(-)/CD33(-)cells increased. The authors concluded that myelokathexis is a disease characterized by the accelerated apoptosis of granulocytes and the depressed expression of bcl-x in bone marrow-derived granulocyte precursor cells. These abnormalities are partially corrected by the in vivo administration of G-CSF. (Blood. 2000;95:320-327)

Adult↗
PubMed2000

Pharmacological characterization of neurogenic responses of the sheep isolated internal anal sphincter.

The aim of the study was to establish the nature of the neurogenic responses of the sheep isolated anal sphincter. Isolated strips of sheep internal anal sphincter develop intrinsic contractile tone following the application of stretch tension. On transmural stimulation (1 - 20 Hz, 10 V pulse strength, 0.5 ms pulse width, 1 s every 180 s) transient relaxations were observed. The amplitude of the relaxations were frequency-dependent reaching a maximal response at 10 - 20 Hz and were inhibited by tetrodotoxin (0.3 microM). Neither atropine (0.3 microM) nor phentolamine (1 microM) affected control responses. The nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 100 microM) and the selective inhibitor of soluble guanylyl cyclase ODQ, (1H-[1,2, 4]oxadiazolo[4,3-a]quinoxalin-1-one) (1 microM) completely inhibited the neurogenic relaxations and uncovered contractions that were abolished by 1 microM phentolamine and 0.1 microM prazosin. The effect of L-NAME, but not that of ODQ, was partially reversed by the addition of L-arginine (1 mM). Sodium nitroprusside (10 nM - 10 microM) caused concentration-dependent inhibition of myogenic tone and this effect was significantly reduced by ODQ. Calcium-free Krebs-Henseleit solution also reduced myogenic tone by 85%. Transmural electrical stimulation of the sheep isolated internal anal sphincter causes a transient relaxation of myogenic tone that appears to involve nitric oxide from non-adrenergic, non-cholinergic nerves and, to a lesser degree, noradrenaline from sympathetic nerves. The characteristics of the preparation compares well with that of human tissue and may prove to be a suitable animal based model for further studies.

Anal Canal↗
PubMed2000

Assessment of pseudohypertrophy as a measure of left-ventricular compression in patients with cardiac tamponade.

BACKGROUND: Left-ventricular pseudohypertrophy reflecting left-ventricular compression was reported in a selected group of patients with cardiac tamponade. HYPOTHESIS: Criteria for the presence of pseudohypertrophy can be established to guide its use as a sign of left-ventricular compression in patients with cardiac tamponade. METHODS: Left-ventricular wall thickness, diameters, relative diastolic wall thickness (%) = (posterior wall thickness/end diastolic radius) x 100 and estimated left-ventricular mass were measured in patients with small, moderate and large pericardial effusion, in patients with cardiac tamponade before and after pericardiocentesis (16 patients in each group) and in 30 control subjects with normal echocardiograms. RESULTS: Left-ventricular posterior wall thickness was increased (12 +/- 2 vs. 9 +/- 1 mm, p < 0.001), left-ventricular end-diastolic diameter was reduced (3.9 +/- 0.5 vs. 4.6 +/- 0.3 cm, p < 0.001) and relative left-ventricular diastolic wall thickness was increased (61 +/- 13 vs. 41 +/- 4.5%, p < 0.001) only in patients with cardiac tamponade compared to controls, but not in patients with small, moderate and large effusions, respectively (relative wall thickness: 42 +/- 5, 41 +/- 7 and 44 +/- 7%, p = NS). Mean values of the estimated left-ventricular mass were similar in all groups. Following pericardiocentesis all parameters were normal. CONCLUSIONS: Despite normal left-ventricular mass, relative left-ventricular diastolic wall thickness is elevated in patients with cardiac tamponade. In contrast it is normal in patients with various degrees of pericardial effusion supporting its use as a quantitative measure of left-ventricular compression in patients with suspected cardiac tamponade.

Adult↗
PubMed1999

Soluble Fas ligand induces epithelial cell apoptosis in humans with acute lung injury (ARDS).

The goals of this study were to determine whether the Fas-dependent apoptosis pathway is active in the lungs of patients with the acute respiratory distress syndrome (ARDS), and whether this pathway can contribute to lung epithelial injury. We found that soluble Fas ligand (sFasL) is present in bronchoalveolar lavage (BAL) fluid of patients before and after the onset of ARDS. The BAL concentration of sFasL at the onset of ARDS was significantly higher in patients who died. BAL from patients with ARDS induced apoptosis of distal lung epithelial cells, which express Fas, and this effect was inhibited by blocking the Fas/FasL system using three different strategies: anti-FasL mAb, anti-Fas mAb, and a Fas-Ig fusion protein. In contrast, BAL from patients at risk for ARDS had no effect on distal lung epithelial cell apoptosis. These data indicate that sFasL is released in the airspaces of patients with acute lung injury and suggest that activation of the Fas/FasL system contributes to the severe epithelial damage that occurs in ARDS. These data provide the first evidence that FasL can be released as a biologically active, death-inducing mediator capable of inducing apoptosis of cells of the distal pulmonary epithelium during acute lung injury.

Apoptosis↗
PubMed1999

Relation of early and one-year outcome after acute myocardial infarction to systemic arterial blood pressure on admission.

We evaluated whether elevated blood pressure (BP) levels with an acute myocardial infarction (AMI) affect the in-hospital course, short-term, and 1-year outcome. Data were derived from a nationwide survey of 2,212 consecutive patients with AMI. Patients were stratified into 3 groups according to admission BP levels: 1,320 patients had normal BP, 840 patients had high BP, and 52 patients had excessive BP. In-hospital (7 days) course, short-term (30 days), and 1-year outcome was compared between the groups. The 3 groups were similar with respect to age, but patients with excessive BP were more likely to be women and have a history of systemic hypertension and diabetes mellitus. The rate of thrombolytic therapy was similar among the 3 groups, but patients with excessively elevated BP were treated during hospitalization much more often with beta blockers, angiotensin-converting enzyme inhibitors, and diuretics. The incidence of stroke, transient ischemic attack, and bleeding complications were comparable in the 3 groups. In-hospital mortality was 5.0% , 4.0%, and 1.9% in the normal, high, and excessively elevated BP groups, respectively (p = 0.19). The short-term rehospitalization or mortality rate was similar among the 3 groups. The 1-year mortality rate was 12.3%, 14.1%, and 10.2% in the normal, high, and excessively elevated BP groups, respectively (p = 0.61). A multivariate logistic regression analysis yielded age, women, and Killip class > or = 2 as the only significant predictors of mortality during follow-up. Thus, with the current medical therapy, excessively elevated BP levels with AMI is not associated with a worse short-term or 1-year outcome.

Adrenergic beta-Antagonists↗
PubMed1999

Are coronary patients at higher risk with digoxin therapy? An ongoing controversy.

Previous reports have yielded contradictory conclusions regarding the safety of digoxin therapy in patients with acute myocardial infarction. The purpose of our study was to determine whether digoxin therapy is associated with increased mortality in patients with chronic coronary artery disease. We analyzed data from 8173 patients who were screened for participation in the Bezafibrate Infarction Prevention (BIP) trial and who survived an acute myocardial infarction at least 6 months prior to the study. Three-year overall mortality of the 451 (15.5%) patients receiving digoxin (according to the judgement of their treating physician) at the time of screening for BIP participation, was 22.4% compared to 8.3% in the patients who did not receive digoxin. Cardiac mortality was 16.2% in the digoxin-treated group, compared to 4.9% in the non-treated patients. The increased risk associated with digoxin remained statistically significant when patients were stratified according to sex, age groups, functional capacity and the presence of hypertension, diabetes or angina. The administration of digoxin to survivors of an acute myocardial infarction in the chronic phase of their disease, is statistically associated with a 30-50% increase in the risk of overall and cardiac mortality during long-term follow-up. A propensity of increased risk of arrhythmias in ischemic coronary patients may explain this finding.

Cardiotonic Agents↗
PubMed1999

Lateral internal sphincterotomy is not redundant in the era of glyceryl trinitrate therapy for chronic anal fissure.

Lateral internal sphincterotomy has been the standard treatment for chronic anal fissure, but fissure healing rates of up to 80% with topical glyceryl trinitrate (GTN) treatment have suggested that this operation may become redundant. We evaluated the results of topical treatment of chronic anal fissures with 0.2% GTN for 6 weeks in the outpatient clinical setting, outside the confines of a randomized clinical trial. The role of lateral internal sphincterotomy in the GTN era was also assessed. GTN induced fissure healing in 21 of 49 consecutive patients. Fissures healed spontaneously in 2 patients who discontinued GTN because of headache. Lateral internal sphincterotomy was performed in 26 patients who had persistent symptoms after 6 weeks of GTN therapy. At the 6-week post-sphincterotomy review, all fissures had healed and there were no complications. In this study topical GTN for treatment of chronic anal fissure in the outpatient setting was not as effective as demonstrated in controlled clinical trials. Lateral internal sphincterotomy is still a good therapeutic option, especially in patients not responding to GTN.

Adult↗
PubMed1998

Prognostic significance of cerebrovascular disease in 11,526 chronic coronary artery disease patients. Bezafibrate Infarction Prevention (BIP) Study Group.

Patients with chronic CAD and a history of cerebrovascular events were compared with patients without prior cerebrovascular events to assess the effect of these events on 5-year prognosis. Despite adjustment for older age and higher comorbidity among patients who had experienced a cerebrovascular event, a history of such an event was associated with an increased risk of 1.86 for total mortality.

Aged↗
PubMed1998

Differentiation of cultured keratinocytes promotes the adherence of Streptococcus pyogenes.

Based on a consideration of the histopathology of nonbullous impetigo that shows localization of Streptococcus pyogenes to highly differentiated, subcorneal keratinocytes, we hypothesized that adherence of an impetigo strain of S. pyogenes would be promoted by terminal differentiation of keratinocytes. An assay was developed in which S. pyogenes adhered via pilus-like projections from the cell wall to the surface of cultured human keratinocytes in a time- and inoculum-dependent manner suggestive of a receptor-mediated process. Terminal differentiation of keratinocytes was induced by increasing the calcium concentration in the growth medium, and was confirmed by morphologic analysis using electron microscopy. Adherence of S. pyogenes was three and fourfold greater to keratinocytes differentiated in 1.0 and 1.5 mM calcium, respectively, compared with undifferentiated keratinocytes in 0.15 mM calcium. The presence of calcium during the adherence assay further enhanced adherence nearly twofold. Adherence occurred preferentially to sites of contact between adjacent keratinocytes, suggesting that the keratinocyte receptor may be a molecule involved in cell-to-cell adhesion. In contrast, nonpathogenic Streptococcus gordonii adhered poorly to keratinocytes regardless of their state of terminal differentiation, and adherence of a pharyngeal strain of S. pyogenes was twofold greater to undifferentiated than differentiated keratinocytes. This is the first report of in vitro adherence of S. pyogenes to keratinocytes in a manner that emulates human impetigo. Adherence of only the impetigo strain, and not the pharyngeal strain of S. pyogenes or the nonpathogenic S. gorgonii isolate, was promoted by keratinocyte differentiation. This result provides a model system for investigating the molecular pathogenesis of streptococcal skin infections.

Bacterial Adhesion↗
PubMed1998

Nifedipine and cancer mortality: ten-year follow-up of 2607 patients after acute myocardial infarction.

Recent publications contended that the use of short-acting calcium antagonists may double the risk of cancer incidence and possibly increase mortality in hypertensive patients. The purpose of this study was to assess the risk ratio for cancer mortality associated with nifedipine in a large population of patients post-myocardial infarction. Cancer mortality data, over a 10-year period, were obtained on 2607 hospital survivors of acute myocardial infarction who were screened, but not included, in the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT I) study. In this group of patients, 526 (20%) were on nifedipine, according to their treating physicians' decision. In the cohort of screened patients not included in SPRINT I, there were 22 (4.2%) cancer-related deaths in the patients on nifedipine compared with 114 (5.5%) in the group not treated with nifedipine (P = 0.23). In multivariate analysis, the 10-year cancer mortality risk ratio associated with nifedipine therapy was 1.06 (95% CI 0.52-2.18). The current analysis shows no evidence of an increased risk of cancer mortality in a large number of patients treated at baseline with nifedipine.

Aged↗