Ismo contains isosorbide mononitrate, a vasodilator used in the management of angina pectoris, coronary heart disease, heart failure, and hypertension. The active ingredient belongs to a long-established category of cardiac therapy whose role is to widen blood vessels and reduce the workload on the heart, addressing the underlying mechanics behind several common cardiovascular conditions.
Within the broader cardiovascular pharmacopoeia, isosorbide mononitrate is grouped with antianginal and antihypertensive agents and is also described in the source data as a medication that reduces pressure in the pulmonary circulation. The structured indication list further down this page details the specific registered uses recognised in the markets where Ismo is sold, and the conditions it is prescribed for largely overlap with chronic, long-term cardiac care rather than acute crisis intervention.
Ismo is registered in 14 countries with a notably wide geographical spread — examples include Germany, India, Chile, Taiwan, Egypt, and New Zealand. That distribution pattern means a traveller or expatriate may encounter the brand in markets as different as Northern Europe, South America, South Asia, and Sub-Saharan Africa. Even so, the brand is not present everywhere, and the same isosorbide mononitrate molecule circulates worldwide under a number of other commercial names.
Other vasodilators and antianginal agents are available internationally under different active ingredients, and a local pharmacist is well placed to identify what is on the regional formulary. Because cardiovascular therapy is closely tailored to the individual patient, any decision to begin, change, or substitute Ismo should be taken with the prescribing healthcare provider rather than improvised across borders.
The ill effects of isosorbide mononitrate overdose are generally the results of isosorbide mononitrate's capacity to induce vasodilatation, venous pooling, reduced cardiac output, and hypotension. These hemodynamic changes may have protean manifestations, including increased intracranial pressure, with any or all of persistent throbbing headache, confusion, and moderate fever; vertigo; palpitations; visual disturbances; nausea and vomiting (possibly with colic and even bloody diarrhea); syncope (especially in the upright posture); air hunger and dyspnea, later followed by reduced ventilatory effort; diaphoresis, with the skin either flushed or cold and clammy; heart block and bradycardia; paralysis; coma; seizures and death. Laboratory determinations of serum levels of isosorbide mononitrate and its metabolites are not widely available, and such determinations have, in any event, no established role in the management of isosorbide mononitrate overdose. There are no data suggesting what dose of isosorbide mononitrate is likely to be life-threatening in humans. In rats and mice, there is significant lethality at doses of 2000 mg/kg and 3000 mg/kg, respectively. No data are available to suggest physiological maneuvers (e.g., maneuvers to change the pH of the urine) that might accelerate elimination of isosorbide mononitrate. In particular, dialysis is known to be ineffective in removing isosorbide mononitrate from the body. No specific antagonist to the vasodilator effects of isosorbide mononitrate is known, and no intervention has been subject to controlled study as a therapy of isosorbide mononitrate overdose. Because the hypotension associated with isosorbide mononitrate overdose is the result of venodilatation and arterial hypovolemia, prudent therapy in this situation should be directed toward an increase in central fluid volume. Passive elevation of the patient's legs may be sufficient, but intravenous infusion of normal saline or similar fluid may also be necessary. The use of epinephrine or other arterial vasoconstrictors in this setting is likely to do more harm than good. In patients with renal disease or congestive heart failure, therapy resulting in central volume expansion is not without hazard. Treatment of isosorbide mononitrate overdose in these patients may be subtle and difficult, and invasive monitoring may be required.
MethemoglobinemiaMethemoglobinemia has been reported in patients receiving other organic nitrates, and it probably could also occur as a side effect of isosorbide mononitrate. Certainly nitrate ions liberated during metabolism of isosorbide mononitrate can oxidize hemoglobin into methemoglobin. Even in patients totally without cytochrome b5 reductase activity, however, and even assuming that the nitrate moiety of isosorbide mononitrate is quantitatively applied to oxidation of hemoglobin, about 2 mg/kg of isosorbide mononitrate should be required before any of these patients manifests clinically significant ( > 10%) methemoglobinemia. In patients with normal reductase function, significant production of methemoglobin should require even larger doses of isosorbide mononitrate. In one study in which 36 patients received 2 to 4 weeks of continuous nitroglycerin therapy at 3.1 to 4.4 mg/hr (equivalent, in total administered dose of nitrate ions, to 7.8 to 11.1 mg of isosorbide mononitrate per hour), the average methemoglobin level measured was 0.2%; this was comparable to that observed in parallel patients who received placebo. Notwithstanding these observations, there are case reports of significant methemoglobinemia in association with moderate overdoses of organic nitrates. None of the affected patients had been thought to be unusually susceptible.
Methemoglobin levels are available from most clinical laboratories. The diagnosis should be suspected in patients who exhibit signs of impaired oxygen delivery despite adequate cardiac output and adequate arterial pO2. Classically, methemoglobinemic blood is described as chocolate brown, without color change on exposure to air. When methemoglobinemia is diagnosed, the treatment of choice is methylene blue, 1 to 2 mg/kg intravenously.
Dosing regimens for most chronically used drugs are designed to provide plasma concentrations that are continu-ously greater than a minimally effective concentration. This strategy is inappropriate for organic nitrates. Several well-controlled clinical trials have used exercise testing to assess the antianginal efficacy of continuously delivered nitrates. In the large majority of these trials, active agents were indistinguishable from placebo after 24 hours (or less) of continuous therapy. Attempts to overcome tolerance by dose escalation, even to doses far in excess of those used acutely, have consistently failed. Only after nitrates have been absent from the body for several hours has their antianginal efficacy been restored. The drug-free interval sufficient to avoid tolerance to isosorbide mononitrate has not been completely defined. In the only regimen of twice-daily isosorbide mononitrate that has been shown to avoid development of tolerance, the two doses of Ismo (isosorbide mononitrate) tablets are given 7 hours apart, so there is a gap of 17 hours between the second dose of each day and the first dose of the next day. Taking account of the relatively long half-life of isosorbide mononitrate this result is consistent with those obtained for other organic nitrates. The same twice-daily regimen of Ismo (isosorbide mononitrate) tablets successfully avoided significant rebound/withdrawal effects. The incidence and magnitude of such phenomena have appeared, in studies of other nitrates, to be highly dependent upon the schedule of nitrate administration.
In humans, isosorbide mononitrate is not subject to first pass metabolism in the liver. The absolute bioavailability of isosorbide mononitrate from Ismo (isosorbide mononitrate) tablets is nearly 100%. Maximum serum concentrations of isosorbide mononitrate are achieved 30 to 60 minutes after ingestion of Ismo. The volume of distribution of isosorbide mononitrate is approximately 0.6 L/kg, and less than 4% is bound to plasma proteins. It is cleared from the serum by denitration to isosorbide; glucuronidation to the mononitrate glucuronide; and denitration/hydration to sorbitol. None of these metabolites is vasoactive. Less than 1% of administered isosorbide mononitrate is eliminated in the urine. The overall elimination half-life of isosorbide mononitrate is about 5 hours; the rate of clearance is the same in healthy young adults , in patients with various degrees of renal, hepatic, or cardiac dysfunction, and in the elderly. In a single-dose study, the pharmacokinetics of isosorbide mononitrate were dose-proportional up to at least 60 mg.
Ismo is prescribed in the management of angina pectoris, coronary heart disease, heart failure, and hypertension. As a vasodilator, it belongs to a category of cardiac therapy used to reduce the workload on the heart and ease symptoms associated with restricted coronary blood flow. The structured indication block further down this page sets out the specific registered uses recognised in the markets where Ismo is sold.
Ismo contains isosorbide mononitrate, classified as a vasodilator with antianginal and antihypertensive properties. The same active ingredient is sold internationally under a number of different brand names, particularly in markets where the original patent has long expired and several manufacturers produce isosorbide mononitrate preparations in parallel for cardiovascular use.
Ismo is registered in 14 countries spread across several regions, including Germany, India, Chile, Taiwan, Egypt, New Zealand, and the United States. The footprint is broad geographically rather than concentrated in one region. If your country is not listed here, a local pharmacist can usually confirm whether isosorbide mononitrate is sold locally under another brand name.
Isosorbide mononitrate is marketed under several brand names worldwide, and other vasodilators used in cardiac therapy also exist within the broader nitrate and antianginal categories. These are not freely interchangeable — molecules and formulations within the class differ in onset, duration, and clinical positioning. To identify a regional equivalent, search the active ingredient on Pill2Trip or ask a pharmacist in your country.
Yes. Ismo is a prescription medication, and nitrate-based cardiac therapy is calibrated to a patient's individual cardiovascular history, concurrent medications, and overall clinical picture. This matters especially for travellers and people relocating between countries, since prescription rules, available brands, and generic equivalents differ between regulatory systems. Any decision to start, stop, or substitute isosorbide mononitrate should be led by a healthcare provider.
