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PubMed2003

Non surgical therapy for anal fissure.

BACKGROUND: Because of the disability associated with surgery for anal fissure and the risk of incontinence, medical alternatives for surgery have been sought. Most recently, pharmacologic methods that relax the anal smooth muscle, to accomplish reversibly what occurs in surgery, have been used to obtain fissure healing. OBJECTIVES: To assess the efficacy and morbidity of various medical therapies for anal fissure. SEARCH STRATEGY: Search terms include "anal fissure randomized". SELECTION CRITERIA: Studies in which participants were randomized to a non-surgical therapy for anal fissure. Comparison groups may include an operative procedure, an alternate medical therapy or placebo. Chronic fissure, acute fissure and fissure in children are included in the review. Atypical fissures associated with inflammatory bowel disease or cancer or anal infection are excluded. DATA COLLECTION AND ANALYSIS: Data were abstracted from published reports and meeting abstracts, assessing method of randomization, blinding, "intention to treat" and drop-outs, therapies, supportive measures (applied to both groups), dosing and frequency and cross-overs. Dichotomous outcome measures included Non-healing of the fissure (a combination of persistence and recurrence), and Adverse events (including incontinence, headache, infection, anaphylaxis). Continuous outcome measures included measures of pain relief and anorectal manometry. MAIN RESULTS: 21 different comparisons of the ability of medical therapies to heal anal fissure have been reported in 31 RCTs. Nine agents were used (nitroglycerin ointment (GTN), isosorbide dinitrate, Botulinum toxin (Botox), diltiazem, nifedipine (Calcium channel blockers or Cachablos), hydrocortisone, lignocaine, bran, placebo) as well as anal dilators and surgical sphincterotomy. When two studies are excluded from analysis due to quality concerns, the significance disappears in the three main analyses: GTN vs. placebo group (0.78; 0.56-1.08), in children (0.96; 0.48-1.92) and adults (0.73; 0.50-1.07). That is, GTN was, in this modified analysis, not significantly better than placebo in curing anal fissure. Cachablos were not tested against placebo, but in a comparison to GTN, Cachablo was equivalent in its ability to cure fissure (odds ratio 0.66; 0.22-2.01). Botox, in a meta-analysis of two studies compared to placebo, showed no significant advantage in efficacy (0.75; 0.32-1.77), and in a comparison to GTN analyzing two studies, was also not significantly better than GTN (0.48; 0.21-1.10). REVIEWER'S CONCLUSIONS: Medical therapy for chronic anal fissure, acute fissure and fissure in children may be applied with a chance of cure that is only marginally better than placebo, and, for chronic fissure in adults, far less effective than surgery.

Fissure in Ano↗
PubMed2006

Non surgical therapy for anal fissure.

BACKGROUND: Because of the disability associated with surgery for anal fissure and the risk of incontinence, medical alternatives for surgery have been sought. Most recently, pharmacologic methods that relax the anal smooth muscle, to accomplish reversibly what occurs in surgery, have been used to obtain fissure healing. OBJECTIVES: To assess the efficacy and morbidity of various medical therapies for anal fissure. SEARCH STRATEGY: Search terms include "anal fissure randomized". Timing from 1966 to May 2006. Further details of the search below. SELECTION CRITERIA: Studies in which participants were randomized to a non-surgical therapy for anal fissure. Comparison groups may include an operative procedure, an alternate medical therapy or placebo. Chronic fissure, acute fissure and fissure in children are included in the review. Atypical fissures associated with inflammatory bowel disease or cancer or anal infection are excluded. DATA COLLECTION AND ANALYSIS: Data were abstracted from published reports and meeting abstracts, assessing method of randomization, blinding, "intention to treat" and drop-outs, therapies, supportive measures (applied to both groups), dosing and frequency and cross-overs. Dichotomous outcome measures included Non-healing of the fissure (a combination of persistence and recurrence), and Adverse events (including incontinence, headache, infection, anaphylaxis). Continuous outcome measures included measures of pain relief and anorectal manometry. MAIN RESULTS: 48 different comparisons of the ability of medical therapies to heal anal fissure have been reported in 53 RCTs. Eleven agents were used (nitroglycerin ointment (GTN), isosorbide dinitrate, Botulinum toxin (Botox), diltiazem, nifedipine (Calcium channel blockers or CCBs), hydrocortisone, lignocaine, bran, minoxidil, indoramin, and placebo) as well as anal dilators and surgical sphincterotomy.GTN was found to be marginally but significantly better than placebo in healing anal fissure (48.6% vs. 37%, p < 0.004), but late recurrence of fissure was common, in the range of 50% of those initially cured. Botox and CCBs were equivalent to GTN in efficacy with fewer adverse events. No medical therapy came close to the efficacy of surgical sphincterotomy, though none in these RCTs was associated with the risk of incontinence. AUTHORS' CONCLUSIONS: Medical therapy for chronic anal fissure, acute fissure and fissure in children may be applied with a chance of cure that is marginally better than placebo, and, for chronic fissure in adults, far less effective than surgery.

Fissure in Ano↗
PubMed1980

Refractory variant angina controlled with combined drug therapy in a patient with a single coronary artery.

A young man with a single left coronary artery and refractory variant angina is described. Spontaneous coronary artery spasm developed during coronary arteriography at the site of a 50% fixed left anterior descending coronary artery stenosis. Frequent episodes of rest angina with transient ST segment elevation persisted in hospital in spite of treatment with three different calcium antagonist drugs. Symptoms disappeared only when the combination of nifedipine, diltiazem, isosorbide dinitrate, and nitroglycerin ointment were given. Ergonovine testing was used to objectively assess the response to treatment.

Adult↗
PubMed1990

Postoperative angiographic evaluation of gastroepiploic artery grafts: technical considerations and short-term patency.

Follow-up angiography was performed in 37 patients with right gastroepiploic artery (GEA) grafts at 27 +/- 32 days postoperatively. By the femoral approach, a 5F cobra or twist catheter was advanced selectively into the gastroduodenal artery (GDA) over a plastic-coated guidewire. In 29 patients, the GDA was successfully catheterized, and the GEA grafts were clearly visualized by the injection of 3-7 ml of contrast medium. GDA catheterization was unsuccessful in 8 patients, but in 4 of them the grafts were well visualized when 15-20 ml of contrast was injected. In the other 4 patients, visualization of the GEA grafts was poor, but the distal portions were outlined by retrograde perfusion from the native right coronary arteries. A total of 34 GEA grafts were patent (92%), and the diameters of these grafts were adequate when compared with respective recipient coronary arteries (2.8 +/- 0.9 and 2.3 +/- 0.6 mm, respectively; P less than .05). No complications were noted except for transient vasospasm (3 patients) in the GEA, hepatic artery, or both, which was relieved by the intra-arterial injection of isosorbide dinitrate (2.5 mg). Thus, the over-the-wire technique allows simple and safe GDA catheterization, which is essential for obtaining good visualization of GEA grafts.

Adult↗
PubMed1984

Clinical characteristics and prognosis of patients with postinfarction angina caused by coronary artery spasm.

Clinical features and the course of 15 patients with postinfarction angina caused by coronary artery spasm are described. Episodes of postinfarction angina in the patients recurred at rest in the early recovery phase and were accompanied by transient ST-segment elevation. The area where ST-segment elevations were demonstrated on a 12-lead ECG always included the leads with newly developed abnormal Q waves. Pain resolved spontaneously or after sublingual nitroglycerin in several minutes. Holter ECGs during a 24-h period demonstrated frequent episodes of ST-segment elevation that were not always associated with chest pain. Treatment with calcium antagonist and/or nitrates effectively suppressed angina, and only one patient developed reinfarction. The patient's subjective symptoms were abolished by diltiazem and isosorbide dinitrate. A Holter ECG of the patient revealed silent ST-segment elevations before and after the reinfarction and an increase of the drugs completely suppressed the recurrence of silent ischemic ECG changes. Coronary arteriograms were obtained from 8 patients, which demonstrated more than 75% segmental stenosis on one coronary artery in 5 patients and no significant obstruction in the remaining 3. All patients performed a treadmill exercise stress test before discharge and most demonstrated excellent tolerance. All patients experienced no form of chest pain for an average of 25 months follow-up under medication. We conclude that among patients with postinfarction angina, those cases caused by coronary artery spasm have a relatively good prognosis.

Adult↗
PubMed1987

Effect of captopril on left ventricular end-systolic pressure-volume and stress-shortening relations in severe cardiac failure.

The effects of captopril on cardiovascular dynamics and left ventricular (LV) contractility were studied in 11 patients with severe congestive heart failure and very poor global LV function. Pressures were measured using a flow-guided catheter, cardiac output by thermodilution, and LV contraction and ejection fraction by simultaneous radionuclide angiography. Ventricular loading conditions were altered by sublingual isosorbide dinitrate to facilitate construction of LV pressure-volume and stress-shortening curves. Captopril decreased mean arterial pressure (p less than 0.02) and systemic vascular resistance, while stroke and cardiac index increased in most patients. Left ventricular ejection fraction increased from 18 +/- 5 to 22 +/- 7% (p less than 0.05), but contractility, assessed from end-systolic pressure-volume and end-systolic pressure-shortening relations, was unchanged or decreased slightly. Heart rate and double product also tended to decrease. In contrast, arteriovenous oxygen difference widened and calculated total oxygen consumption increased during captopril therapy (p less than 0.05). The study showed that captopril improved forward blood flow, total oxygen extraction, and LV ejection fraction following the decrease impedance to LV emptying but not at the expense of an increase in ventricular contractility. This makes captopril an attractive drug for patients with end-stage cardiac failure and a severely damaged myocardium.

Aged↗
PubMed1987

Chronic Chagas' heart disease presenting as an impending myocardial infarction: a case favoring the neurogenic pathogenesis concept.

A 55-year-old Caucasian woman suddenly developed substernal chest pain at rest accompanied by pallor, diaphoresis, nausea, and vomiting. Physical examination was otherwise unremarkable. The resting ECG showed T-wave inversion in all anterior leads which returned to normal 24 h after the onset of the symptoms. The pain was eliminated promptly by sublingual isosorbide dinitrate. "Impending" acute myocardial infarction was diagnosed. Coronary arteriography, however, failed to reveal any change in any major coronary artery but an apical aneurysm of the left ventricle was detected. As the complement-fixation test for Chagas' disease was positive, the diagnosis of chronic Chagas' heart disease was then established. This unusual clinical manifestation of Chagas' disease is thought to be the consequence of a transient imbalance in the cardiac autonomic nervous system, which is considered to play a central role in the pathogenesis of chronic Chagas' heart disease. In addition, the present case may alert clinicians to the thus far neglected atypical chest pain, which is frequently seen in chagasic patients but whose etiology remains obscure.

Chagas Cardiomyopathy↗
PubMed1990

The slope of the end-systolic pressure-volume relationship compared with the global end-systolic pressure-volume ratio in humans.

The slope of the end-systolic pressure-volume relationship (Emax), which is generated clinically by load manipulation, as well as the "absolute" peak systolic pressure end-systolic volume ratio (denoted as pressure-volume ratio), have been suggested as indices defining left ventricular function. This study represents an attempt to determine the relationship between these two indices by studying 20 patients (16 with coronary artery disease and 4 with normal coronary arteries) undergoing cardiac catheterization. Left ventriculography was performed three times in each patient: (1) in the control baseline state, (2) after rapid intravenous infusion of 250-300 cc of saline, and (3) after sublingual administration of 5 mg isosorbide dinitrate. Emax was approximated by linear regression using the peak left ventricular pressure (replacing end-systolic pressure) and the smallest left ventricular (end-systolic) volume for these three different loads. Acute ischemia with typical chest pain and ECG changes developed in 4 patients during saline loading. The pressure-volume ratio showed no change with load manipulation in patients who did not demonstrate ischemia. In the 4 patients who developed acute ischemia, the pressure-volume ratio dropped from 4.4 +/- 1.3 to 2.9 +/- 0.9 mmHg/ml (p less than 0.001). In all of the patients, the pressure-volume ratio, but not the Emax, correlated with the ejection fraction (r = 0.6; p less than 0.05). In addition, the Emax line demonstrated a markedly nonphysiological Vo. There was no correlation between Emax and pressure-volume ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Coronary vasospasm as a potential cause of myocardial infarction and paroxysmal atrial fibrillation in a relatively young woman.

Vasospasm-related myocardial infarction in young women with normal coronary arteries has infrequently been reported and vasospasm-related paroxysmal atrial fibrillation (PAF) has rarely been described. We present a 33-year-old woman with old inferior myocardial infarction and postinfarction angina at rest; the angina was accompanied by PAF and electrocardiographic ST-segment elevation in the inferior leads. Coronary angiography revealed normal coronary arteries and intracoronary acetylcholine provoked an intense and diffuse spasm of the right and left coronary artery. The spasm of the right coronary artery was associated with PAF and ST-segment elevation in the inferior leads. Frequently documented PAF, accompanied by chest discomfort and ST-segment elevation in the inferior leads, was more effectively removed with isosorbide dinitrate than with disopyramide. These data suggest that coronary vasospasm is a likely cause of myocardial infarction and even PAF, although the precise mechanism leading to PAF remains unknown.

Acetylcholine↗
PubMed1995

Critical review of heart failure: the role of left ventricular remodeling in the therapeutic response.

Recent clinical investigations have provided new insights into physiologic alterations taking place as heart failure progresses. As a result, new end points may be more relevant to monitor in patients, rather than the classical assessment of severity based on subjective evaluation of functional capacity. Structural changes of the myocardium, referred to as remodeling, have profound effects on the performance of the left ventricle and on long-term prognosis. Left ventricular ejection fraction may serve as a clinical marker for remodeling changes. Remodeling changes involve hypertrophy of the muscle mass, dilation of the left ventricle, and a change in the shape of the ventricle. Histologically, these changes are produced by myocyte lengthening, interstitial growth, and myocyte slippage. The consequences of remodeling include an abnormal bio-energetic state because of the augmented wall stress and accentuated myocardial oxygen consumption. The elevated wall stress promotes further hypertrophy. Superimposed on the remodeling changes is neurohormonal activation. Both remodeling and neurohormonal activation are directly related to mortality. An experimental canine model has been used successfully to investigate the potential impact of pharmacologic intervention on remodeling. Angiotensin-converting enzyme inhibitors and the combination of hydralazine and isosorbide dinitrate have been shown in clinical trials to reduce long-term mortality and increase ejection fraction. The effects of these drugs appear to be mediated in part by alterations in remodeling and neurohormonal activation. Thus, left ventricular ejection fraction can be used as a clinical marker for remodeling processes, and plasma norepinephrine levels can be used as a marker for neurohormonal activation.

Animals↗
PubMed1996

Pharmacologic treatment of congestive heart failure.

Congestive heart failure is a clinical syndrome producing symptomatic deterioration, functional impairment, and shortened life span. The syndrome is complex in that it includes both peripheral and cardiac effects which contribute to the progression of heart failure. In the periphery, elevations in the sympathetic nervous system and renin-angiotensin system increase afterload and contribute to further salt and water retention. The central cardiac abnormalities include remodeling of the heart and downregulation of beta receptors. Traditional heart failure therapy has included treatment of fluid retention with diuretics, although their effect on mortality has never been addressed. The most proven therapy in heart failure is treatment with vasodilators, particularly angiotensin-converting enzyme (ACE) inhibitors. Improved survival with ACE-inhibitor therapy has been demonstrated in patients with severe heart failure (CONSENSUS), mild to moderate heart failure (SOLVD), and in comparison with vasodilator therapy with hydralazine isosorbide dinitrate (VHeFT II). Improved survival has also been noted in postmyocardial infarction when the ejection fraction is decreased (SAVE). The ACE inhibitors have now become standard therapy for heart failure regardless of severity. Additive vasodilator therapy with calcium-channel antagonists is under investigation. Inotropic therapy is controversial at present because of disappointing mortality results. The clinical mainstay digitalis remains without convincing mortality reduction data. Other inotropic agents, particularly phosphodiesterase inhibitors, have shown uniformly negative survival results. However, the new mixed action agents vesnarinone and pimobenden have shown favorable data, with vesnarinone demonstrating a mortality reduction effect. Beta-blocker therapy in heart failure has also found renewed interest, particularly with the new agents carvedolol and bucindolol which also have vasodilating properties.

Drug Therapy, Combination↗
PubMed2000

Dipyridamole-induced reversible thallium-201 defect in patients with vasospastic angina and nearly normal coronary arteries.

BACKGROUND: Dipyridamole is a vasodilator of resistance vessels and has no vasoconstrictive effect on large coronary arteries. HYPOTHESIS: The present study used dipyridamole thallium-201 (201Tl) scintigraphy to clarify the role of microvasculature in coronary flow limitation in patients with vasospastic angina and normal coronary arteries. METHODS: Sixteen patients underwent dipyridamole and exercise 201Tl scintigraphy and provocative coronary angiography with acetylcholine. All patients showed coronary spasm (> 90% vasoconstriction concomitant with ST change) in at least one vessel. RESULTS: Dipyridamole or exercise caused only ST depression despite the ST elevation observed at spontaneous attack. Dipyridamole 201Tl scintigraphy demonstrated the reversible defects (11 cases), as did exercise 201Tl scintigraphy (13 cases). The region of 201Tl defect was not always consistent with the territories of angiographically depicted vasospastic arteries. Basal coronary tone, assessed by percentage of diameter change of epicardial arteries from baseline to isosorbide dinitrate administration, did not differ between the positive and the negative defect regions. CONCLUSION: These results support the hypothesis that, in addition to epicardial coronary spasm, the dysfunction of microvasculature is responsible for abnormal coronary perfusion in the subgroup of patients with vasospastic angina and normal coronary arteries.

Angina Pectoris↗
PubMed2004

Nitric oxide as a radiosensitizer: evidence for an intrinsic role in addition to its effect on oxygen delivery and consumption.

Different nitric oxide (NO)-mediated treatments (e.g., isosorbide dinitrate, insulin and electrical stimulation of the host tissue) have been investigated for their effects on tumor oxygenation and radiation sensitivity. We further address the issue of the role played by modulation of the NO-pathway in tumor radiosensitivity. For this purpose, the local concentration of NO was monitored after treatment in FSaII tumors and a comparison between the sensitivity of LLC tumors implanted both on eNOS(-/-) and wild-type (WT) mice was carried out. First, we demonstrate the central role played by eNOS in the radiosensitizing effect after application of insulin treatment and electrical stimulation: a significant increase in tumor NO content is induced by these treatments and the increase in tumor oxygenation, as well as the radiosensitizing effect are abolished in eNOS knock-out mice, in contrast to WT mice. Second, by comparing the level of oxygen and NO achieved in tumors after NO-mediated treatments and carbogen, we provide evidence that these NO-mediated treatments are not simply acting by a single oxygen effect. These treatments induced significant regrowth delays compared to carbogen, despite a smaller increase in tumor oxygenation. For the NO-mediated treatments, there was a direct correlation between the NO content and the radiosensitizing effect. These data strongly suggest that NO is a complementary factor additive to oxygen in determining the sensitivity to irradiation and we therefore propose that NO acts as an intrinsic radiosensitizer in vivo.

Animals↗
PubMed1978

Improved GLC determination of plasma nitroglycerin concentrations.

A specific and quantitative assay for determining nanogram levels of nitroglycerin in plasma was developed. The method involves stabilization of the drug in plasma with silver nitrate, followed by multiple extraction using purified hexane. Isosorbide dinitrate is added as the internal standard. The hexane extract is subsequently concentrated and injected into a glass column packed with 3% SP-2401 on 100--120-mesh Supelcoport at 140 degrees. A 63Ni-electron-capture detector gives a linear response over the range of 0.1--50 ng of nitroglycerin/ml of rat plasma. From spiked samples, the procedure gave a recovery of about 90%. There was little or no interference from the isomeric glyceryl dinitrates and endogenous compounds in rat or human plasma.

Animals↗
PubMed1983

High-performance liquid chromatographic assay for partially nitrated glycerins in nitroglycerin.

A high-performance liquid chromatographic method for determining the concentration of mononitroglycerins and dinitroglycerins in the commonly used pharmaceutical raw material nitroglycerin (10% w/w) on lactose USP is presented. A coefficient of variation of less than 5% for the partially nitrated glycerins was achieved over the range examined (0-4.0 micrograms/mg). Thirteen lots of raw material were examined and found to contain a total of less than 0.13% w/w partially nitrated glycerins. A variable wavelength detector (lambda = 218 nm) and a microphenyl column were employed. The mobile phase was acetonitrile-water (36:64) pumped at 2 ml/min. The internal standard was isosorbide dinitrate. Total analysis time was 12 min.

Chromatography, High Pressure Liquid↗
PubMed1984

Determination of picogram nitroglycerin plasma concentrations using capillary gas chromatography with on-column injection.

A specific, sensitive, and precise capillary gas chromatographic (GC) assay capable of analyzing picogram concentrations of nitroglycerin in human plasma was developed. The analytical procedure involves a double extraction of 1 mL of plasma with pentane, after the addition of internal standard (1 ng of 2,6-dinitrotoluene), followed by evaporation and reconstitution in 50 microL of heptane. The extract (1 microL) was injected onto a capillary column using the on-column injection technique. The GC oven temperature was programmed from 120 degrees C to 180 degrees C at a rate of 5 degrees C/min. The oven temperature was then programmed to 250 degrees C and was maintained for 10 min. The nitroglycerin and internal standard retention times were 8.6 and 11.4 min, respectively. The position of the end of the capillary column inside the detector is a critical determinant of sensitivity: the column exit must be positioned such that nitroglycerin adsorption to the detector is minimized (i.e., sensitivity maximized). The assay limit of quantitation was 25 pg/mL (CV = 7.6%) using 1 mL of plasma. This GC assay, specific for nitroglycerin in the presence of its metabolites, isosorbide dinitrate, and several other drugs, may be used to quantitate plasma levels obtained after therapeutic nitroglycerin doses.

Chromatography, Gas↗
PubMed2002

Heme oxygenase-1 induction may explain the antioxidant profile of pentaerythrityl trinitrate.

The organic nitrate pentaerythrityl tetranitrate (PETN) is known to exert long-term antioxidant and antiatherogenic effects by as yet unidentified mechanisms. In cultured endothelial cells derived from human umbilical vein, the active PETN metabolite PETriN (0.01-1 mM) increased heme oxygenase (HO)-1 mRNA and protein levels in a concentration-dependent fashion. HO-1 induction was accompanied by a marked increase in catalytic activity of the enzyme as reflected by enhanced formation of carbon monoxide and bilirubin. Pretreatment with PETriN or bilirubin at low micromolar concentrations protected endothelial cells from hydrogen peroxide-mediated toxicity. HO-1 induction and endothelial protection by PETriN were not mimicked by isosorbide dinitrate, another long-acting nitrate. The present study demonstrates that PETriN stimulates mRNA and protein expression as well as enzymatic activity of the antioxidant defense protein HO-1 in endothelial cells. Increased HO-1 expression and ensuing formation of cytoprotective bilirubin may contribute to and explain the specific antioxidant and antiatherogenic actions of PETN.

Animals↗
PubMed1997

The mechanism of inhibition of DNA synthesis in articular chondrocytes from young and old rats by nitric oxide.

The mechanism by which nitric oxide inhibits the incorporation of [3H]thymidine into rat articular chondrocytes (AC) in culture was studied. First-passage articular chondrocytes, isolated by collagenase digestion of cartilage fragments from humeral and femoral heads of 1- and 18-month-old rats, were used in all experiments. NO-generating compounds, isosorbide dinitrate or sodium nitoprusside, inhibited the incorporation of [3H]thymidine and the release of prostaglandin E2 (PGE2) and stimulated cyclic guanosine monophosphate (cGMP) production by rat AC monolayers in a concentration-dependent manner. The cells from old rats were much less sensitive to NO donors and also produced less PGE2 and cGMP. Blocking the production of endogenous NO with NG-monomethyl-L-arginine (L-NMA), an inhibitor of NO synthase, stimulated DNA synthesis. cGMP was found to be a key mediator of the inhibition of DNA synthesis by NO donors in rat AC. 6-Anilino-5,8-quinolinedione (LY83583), an inhibitor of NO-dependent cGMP release, stimulated [3H]-thymidine incorporation, whereas the cGMP analog, 8- bromo-cGMP, inhibited L-NMA-induced or LY83583-induced stimulation of [3H]thymidine incorporation. NO donors blocked the stimulation of DNA synthesis induced by L-NMA and only marginally blocked that of LY83583. Indomethacin had no effect on the inhibition of DNA synthesis by NO or 8-bromo-cGMP. These results show that NO donors induce inhibition of DNA synthesis probably by elevating cGMP. The relative insensitivity of senescent cells to NO donors may be due, at least in part, to their decreased capacity to produce cGMP.

Aging↗

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