Ramipril

What it is

Ramipril is a prescription angiotensin-converting enzyme (ACE) inhibitor, supplied as capsules. It is itself inactive and is converted in the body to ramiprilat, which is the molecule that blocks the enzyme. It is approved in the United States for high blood pressure, for reducing cardiovascular events in people aged 55 and over at high risk, and for heart failure after a heart attack. It carries a boxed warning about fetal toxicity.

What the research says

Ramipril lowers blood pressure and, in two large placebo-controlled outcome trials, lowered the risk of dying. In HOPE, 9,297 high-risk people aged 55 and over had the combined rate of heart attack, stroke or cardiovascular death cut from 17.8% to 14.0% over a mean of five years, and death from any cause from 12.2% to 10.4%. In AIRE, 2,006 people with heart failure after a heart attack had all-cause mortality cut from 23% to 17%. Against that it causes cough in a substantial minority, carries a small but real risk of angioedema that is higher in Black patients, raises potassium, and can injure or kill a developing fetus. It did not prevent diabetes when tested for that purpose.

Evidence grade: Well established.

How it works

Drug class: Angiotensin-converting enzyme (ACE) inhibitor

Ramipril is converted in the body to ramiprilat, which blocks angiotensin-converting enzyme. That enzyme turns angiotensin I into angiotensin II, a powerful blood-vessel constrictor that also tells the adrenal gland to release aldosterone. Blocking it means less angiotensin II, so blood vessels relax and blood pressure falls, and less aldosterone, which is why serum potassium tends to rise a little. The same enzyme also breaks down bradykinin, and the build-up of bradykinin is the presumed reason for ACE inhibitor cough and angioedema. (Source 1)

Boxed warning

When pregnancy is detected, discontinue ramipril as soon as possible [see Warnings and Precautions (5.6)].

(Source 2)

What it is used for

• Blood-pressure lowering by ACE inhibitors including ramipril is well established, though the size of the effect from a single standard dose is modest. A meta-analysis of 484 placebo-controlled trials in 104,176 participants found monotherapy at standard dose reduced systolic pressure by 8.7 mmHg on average, with each doubling of dose adding only 1.5 mmHg. Evidence: established. (Source 3)
• The HOPE trial randomised 9,297 people aged 55 and over with vascular disease or diabetes plus another risk factor to ramipril 10 mg daily or placebo for a mean of five years. The primary composite endpoint fell from 17.8% to 14.0%, an absolute reduction of 3.8 percentage points or about one event prevented for every 26 people treated for five years, and death from any cause fell from 12.2% to 10.4%. Evidence: established. (Source 4)
• The AIRE trial randomised 2,006 survivors of acute myocardial infarction with clinical heart failure to ramipril or placebo starting day 3 to 10. All-cause mortality was 17% on ramipril versus 23% on placebo, a 27% relative risk reduction and an absolute reduction of about 6 percentage points, roughly one death avoided per 17 people treated over an average 15 months. Evidence: established. (Source 5)
• Tested directly and failed. The DREAM trial randomised 5,269 people with impaired fasting glucose or impaired glucose tolerance to ramipril up to 15 mg daily or placebo for a median three years; the primary outcome of diabetes or death occurred in 18.1% on ramipril versus 19.5% on placebo, hazard ratio 0.91, not significant. Regression to normoglycaemia was more common on ramipril. Evidence: not-supported. (Source 6)
• The headline trial supporting this use, published in JAMA in 2013, was retracted in 2015 after the first author admitted data fabrication. A separate, independent, much smaller randomised trial of 33 patients found ramipril improved maximum treadmill walking distance by an adjusted mean of 131 metres (95% CI 62 to 199, p = 0.001) over 24 weeks, with no improvement in ankle-brachial index. One 33-patient trial is not a literature. Evidence: disputed. (Source 7)

Interactions

• Potassium supplements and other potassium-raising drugs (label): Ramipril already pushes potassium up by cutting aldosterone, so adding a potassium supplement, a potassium-sparing diuretic or another potassium-raising drug can produce hyperkalaemia. In a Danish cohort of people with diabetes, potassium supplement use was about 1.6 times more prevalent among those who developed hyperkalaemia. (Source 8)
• Potassium-based salt substitutes (clinical trial): Salt substitutes replace some sodium chloride with potassium chloride, which is a potassium load in food form. A 2026 network meta-analysis of 34 trials in 37,063 people found these products lower blood pressure and, in one large Chinese trial, mortality, but the reviewers say kidney disease and hyperkalaemia risk should be ruled out first, which is exactly the situation created by an ACE inhibitor. (Source 9)
• NSAIDs including selective COX-2 inhibitors, especially with a diuretic (label): This is the combination clinicians call the triple whammy. The label warns that in elderly, volume-depleted or kidney-impaired people, adding an NSAID to an ACE inhibitor can deteriorate kidney function including possible acute renal failure, and that NSAIDs may blunt the blood-pressure effect. A meta-analysis of five case-control studies found the three-drug combination doubled the odds of acute kidney injury. (Source 10)
• NSAIDs plus a diuretic (observational evidence) (case reports): The pooled observational evidence puts a number on it: the odds of acute kidney injury within 12 months were about twice as high in people exposed to all three drug groups together, though the certainty of that evidence was rated low and heterogeneity was high. Limit: All five studies pooled here are case-control studies, so the figure is an odds ratio and shows an association, not that the drug combination caused the kidney injury. The heterogeneity statistic, written I² and equal to 90 per cent, means the individual studies disagreed strongly with one another, and the authors themselves rate the kidney-injury evidence as low certainty and the mortality evidence as very low certainty. The pooled figure rests on four of the five studies. The authors’ own conclusion also mentions "related hospitalizations", but no hospitalisation result appears anywhere in the paper’s abstract, so that part of their conclusion is not supported by any number they report. (Source 11)
• Sacubitril/valsartan and other neprilysin inhibitors, and aliskiren (label): These are outright contraindications rather than cautions, because combining them with an ACE inhibitor multiplies the angioedema and kidney risks. The label requires a 36-hour gap when switching to or from sacubitril/valsartan. Limit: The label’s own contraindications section breaks off in the middle of its list at "in patients with diabetes", with no second item and no full stop. That is a defect in the published document and has been left exactly as printed. The same label completes the thought in its summary page, where it says not to give aliskiren with ramipril to patients with diabetes. (Source 12)
• Alcohol (theoretical): We found no trial or pharmacokinetic study of a ramipril-alcohol interaction in the literature we searched, and the label's drug interaction sections do not list alcohol. Alcohol lowers blood pressure acutely and could in theory add to ramipril's hypotensive effect, which the label does warn about for first doses in post-infarction heart failure, but that is reasoning rather than evidence. (Source 13)
• Other drugs acting on the renin-angiotensin system, including aliskiren and angiotensin receptor blockers (label): The label tells prescribers to avoid using two renin-angiotensin blockers together, and forbids combining ramipril with aliskiren in anyone with diabetes. The elided section of the label that carries this sits between the potassium warning and the NSAID warning. (Source 14)
• Lithium (case reports): ACE inhibitors can raise lithium levels in the blood and lithium toxicity has been reported, so the label recommends frequent lithium monitoring; adding a diuretic may increase the risk further. (Source 15)
• Injectable gold (sodium aurothiomalate) (case reports): Rarely, people on injectable gold together with an ACE inhibitor have had a reaction of facial flushing, nausea, vomiting and low blood pressure, which the label calls a nitritoid reaction. (Source 16)
• mTOR inhibitors such as temsirolimus, and neprilysin inhibitors such as sacubitril (label): The label states that people taking an mTOR inhibitor or a neprilysin inhibitor at the same time as ramipril may be at increased risk of angioedema, the swelling reaction that can be fatal when it involves the airway. (Source 17)

Stopping it

• The one stopping instruction that is absolute is in the boxed warning: when pregnancy is detected, ramipril is to be discontinued as soon as possible, because drugs acting on the renin-angiotensin system can injure and kill the developing fetus. (Source 2)
• ACE inhibitor cough is a reason people stop, and stopping reliably fixes it. The label states that the persistent dry cough reported with all ACE inhibitors always resolves after discontinuation of therapy, and that cough was the commonest single reason for stopping ramipril in the U.S. hypertension trials. (Source 18)
• Stopping is not free when the drug is being taken for an outcome rather than a symptom. In HOPE, 34% of the ramipril group and 32% of the placebo group discontinued at some point, yet the surviving treatment effect was still a fall in all-cause death from 12.2% to 10.4% over five years, so the benefit being given up by stopping is a mortality benefit, not a blood-pressure number. (Source 19)
• There is no withdrawal syndrome described for ramipril in the literature we searched, and no tapering schedule in the label; what the label does require is observation after the FIRST dose in post-infarction heart failure, because of hypotension on starting rather than on stopping. (Source 13)

What goes wrong

In a network meta-analysis of 135 randomised trials, ACE inhibitors roughly doubled the risk of cough compared with placebo, and the authors concluded that all ACE inhibitors carry a similar cough risk. (Source 20)

• Meta-analysis, Moderate certainty.
• Size: 135 randomised controlled trials with 45,420 patients treated with eleven ACE inhibitors.
• Who: randomised trial participants on ACE inhibitors compared with placebo, angiotensin receptor blockers or calcium channel blockers.
• How long: not stated in the abstract.
• Result: pooled relative risk of cough versus placebo 2.21, 95% CI 2.05-2.39; versus an angiotensin receptor blocker 3.2, 95% CI 2.91-3.51; versus a calcium channel blocker 5.30, 95% CI 4.32-6.50. The eleven ACE inhibitors were also ordered by SUCRA, a ranking probability, from moexipril 80.4% down to spirapril 12.3%, with ramipril at 76.4%; the authors report no head-to-head risk estimates between individual ACE inhibitors.
• Funding: not stated.

Limit of this finding: The percentages next to each drug name are not cough rates and not risks. They are SUCRA values, a statistical ranking score that says how likely each drug is to come out worst in the network, and they are produced mostly by indirect comparison rather than by trials pitting one ACE inhibitor against another. In the same passage the authors state plainly that all ACE inhibitors have a similar cough risk, so ramipril’s position in that list must not be read as evidence that it causes more cough than another ACE inhibitor. The grammatical slip "All ACEI has the similar risk" is the journal’s own.

The pooled estimated relative risk (RR) between ACEI and placebo was 2.21 (95% CI: 2.05-2.39). ACEI had more incidences of cough than ARB (RR 3.2; 95% CI: 2.91, 3.51), and pooled estimated of RR between ACEI and CCB was 5.30 (95% CI: 4.32-6.50) Moexipril ranked as number one for inducing cough (SUCRA 80.4%) and spirapril ranked the least (SUCRA 12.3%). The order for the rest of the ACEIs are as follows: ramipril (SUCRA 76.4%), fosinopril (SUCRA 72.5%), lisinopril (SUCRA 64.7%), benazepril (SUCRA 58.6%), quinapril (SUCRA 56.5%), perindopril (SUCRA 54.1%), enalapril (SUCRA 49.7%), trandolapril (SUCRA 44.6%) and, captopril (SUCRA 13.7%). All ACEI has the similar risk of developing a cough.

In the HOPE trial, cough led to stopping or interrupting treatment in 7% of ramipril patients versus 2% on placebo, and angioedema in 0.3% versus 0.1%. (Source 19)

• Official position, Moderate certainty.
• Size: 9,297 patients (4,645 ramipril, 4,652 placebo)
• Who: HOPE trial participants aged 55 and over at high cardiovascular risk.
• How long: mean 5 years.
• Result: discontinuation at any time 34% versus 32%; cough as a reason for stopping 7% versus 2%; hypotension or dizziness 1.9% versus 1.5%; angioedema 0.3% versus 0.1%. In AIRE, hypotension 11% versus 5%, increased cough 8% versus 4%, abnormal kidney function 1% versus 0.5%.
• Funding: manufacturer's label (position of the sponsor and FDA, SPL effective 2026-09-18)

Limit of this finding: The second table in this passage prints its own caption as "Possibly/ Probably" with a stray space, which is the label’s typography and has been kept. The two tables come from two different trials, HOPE and AIRE, with different populations and different follow-up, so their percentages should not be compared with each other.

Reasons for stopping Cough 2% 7% Hypotension or dizziness 1.5% 1.9% Angioedema 0.1% 0.3%

In a one-year hypertension study behind the label, cough appeared in almost 12% of ramipril patients and about 4% stopped treatment because of it. (Source 21)

• Official position, Moderate certainty.
• Size: over 4,000 patients evaluated for safety in hypertension; the later study was a 1-year study.
• Who: patients with hypertension in controlled trials.
• How long: 1 year.
• Result: increased cough in almost 12% of ramipril patients, with about 4% requiring discontinuation.
• Funding: manufacturer's label (position of the sponsor and FDA, SPL effective 2026-09-18)

In a later 1-year study, increased cough was seen in almost 12% of ramipril patients, with about 4% of patients requiring discontinuation of treatment.

The label states that in controlled trials ACE inhibitors cause a higher rate of angioedema in Black patients than in non-Black patients, but the post-marketing rates it reports did not differ statistically. (Source 17)

• Official position, Low certainty.
• Size: 1,523 Black and 8,680 non-Black patients in a large U.S. post-marketing study.
• Who: patients taking an ACE inhibitor in a large United States post-marketing study.
• How long: not stated.
• Result: angioedema reported in 3/1,523 (0.2%) Black patients and 8/8,680 (0.09%) non-Black patients; the label states these rates were not different statistically; angioedema associated with laryngeal edema can be fatal.
• Funding: manufacturer's label (position of the sponsor and FDA, SPL effective 2026-09-18)

In considering the use of ramipril, note that in controlled clinical trials ACE inhibitors cause a higher rate of angioedema in Black patients than in non-Black patients. In a large U.S. post-marketing study, angioedema (defined as reports of angio, face, larynx, tongue, or throat edema) was reported in 3/1523 (0.2%) Black patients and in 8/8680 (0.09%) non-Black patients. These rates were not different statistically.

The label reports hyperkalaemia above 5.7 mEq/L in about 1% of hypertensive patients on ramipril in clinical trials, mostly as isolated values that resolved on continued treatment. (Source 22)

• Official position, Moderate certainty.
• Size: not stated for this analysis.
• Who: hypertensive patients receiving ramipril in clinical trials.
• How long: not stated.
• Result: hyperkalaemia (serum potassium >5.7 mEq/L) in approximately 1%; no patient discontinued for hyperkalaemia; risk factors renal insufficiency, diabetes mellitus and concomitant potassium-raising drugs.
• Funding: manufacturer's label (position of the sponsor and FDA, SPL effective 2026-09-18)

In clinical trials with ramipril, hyperkalemia (serum potassium >5.7 mEq/L) occurred in approximately 1% of hypertensive patients receiving ramipril.

In a Danish population cohort of people with drug-treated diabetes, one in six developed hyperkalaemia, and ACE inhibitor use and potassium supplement use were both commoner among those who did. (Source 23)

• Cohort study, Low certainty.
• Size: 68,601 individuals with first-time drug-treated diabetes.
• Who: Danish residents starting drug treatment for diabetes, 2000-2012, median age 62.
• How long: mean follow-up 4.1 years.
• Result: 16% experienced hyperkalaemia (potassium >5.0 mmol/l), incidence rate 40 per 1000 person-years; prevalence ratio 1.24, 95% CI 1.20-1.28 for ACE inhibitor use and 1.59, 95% CI 1.52-1.67 for potassium supplements; 6-month mortality after hyperkalaemia 20%, hazard ratio for death versus matched controls 6.47, 95% CI 5.81-7.21.
• Funding: Research Support, Non-U.S. Gov't.

Limit of this finding: This is a Danish national registry cohort of people starting diabetes medicines, so it shows associations rather than causes. Hyperkalaemia here means a single blood potassium above 5.0 mmol per litre, a definition that sits in the part of the paper not quoted, and a result just above that threshold is not the same as a dangerous one.

People who developed hyperkalaemia had a higher prevalence of chronic kidney disease [prevalence ratio 1.74 (95% CI 1.68-1.81)], heart failure [prevalence ratio 2.35 (95% CI 2.18-2.54)], use of angiotensin-converting enzyme inhibitors [prevalence ratio 1.24 (95% CI 1.20-1.28)], use of spironolactone [prevalence ratio 2.68 (95% CI 2.48-2.88)] and potassium supplements [prevalence ratio 1.59 (95% CI 1.52-1.67)].

A systematic review and meta-analysis found that taking an NSAID alongside a renin-angiotensin system inhibitor and a diuretic doubled the odds of acute kidney injury, on low-certainty evidence. (Source 11)

• Systematic review, Low certainty.
• Size: five case-control studies involving 410,130 participants.
• Who: people concomitantly exposed to diuretics, renin-angiotensin-aldosterone system inhibitors and NSAIDs.
• How long: acute kidney injury within 12 months after exposure.
• Result: odds ratio 2.01, 95% CI 1.30-3.10 from four studies, I² 90%, low certainty of evidence; three studies on all-cause mortality showed no significantly higher risk, very low certainty.
• Funding: not stated.

Limit of this finding: All five studies pooled here are case-control studies, so the figure is an odds ratio and shows an association, not that the drug combination caused the kidney injury. The heterogeneity statistic, written I² and equal to 90 per cent, means the individual studies disagreed strongly with one another, and the authors themselves rate the kidney-injury evidence as low certainty and the mortality evidence as very low certainty. The pooled figure rests on four of the five studies. The authors’ own conclusion also mentions "related hospitalizations", but no hospitalisation result appears anywhere in the paper’s abstract, so that part of their conclusion is not supported by any number they report.

The risk of AKI was significantly higher among those exposed to TW vs. not exposed (odds ratio [OR] 2.01, 95% confidence interval [CI] 1.30-3.10; four studies; I²: 90%; low certainty of evidence). Three studies provided data on all-cause mortality, not showing a significantly higher risk with TW exposure (very low certainty of evidence).

A network meta-analysis of short-term blood-pressure trials found that several regimens, including ACE inhibitor combinations, increased treatment discontinuation due to adverse events compared with placebo, while angiotensin receptor blocker regimens reduced it. (Source 24)

• Meta-analysis, Moderate certainty.
• Size: 716 trials with 159,362 participants.
• Who: double-blind randomised trial participants on one of five major antihypertensive classes or their combinations, mean age 54.6, mean baseline blood pressure 158/100 mmHg.
• How long: mean follow-up 8.6 weeks, range 4 to 26 weeks.
• Result: ACE inhibitor plus calcium channel blocker odds ratio for discontinuation 1.46, 95% credible interval 1.13-1.87, risk difference 1.1%, 95% CrI 0.2%-2.4%; angiotensin receptor blocker monotherapy OR 0.73, 95% CrI 0.61-0.86, risk difference -0.8%; all regimens significantly increased dizziness.
• Funding: not stated in the abstract.

Compared with placebo, treatment discontinuation due to AEs was significantly increased by CCBs (OR, 1.43 [95% CrI, 1.23-1.67]; risk difference [RD], 1.2% [95% CrI, 0.6%-2.0%]), angiotensin-converting enzyme inhibitors plus CCBs (OR, 1.46 [95% CrI, 1.13-1.87]; RD, 1.1% [95% CrI, 0.2%-2.4%]), and β-blockers plus thiazide diuretics (OR, 1.58 [95% CrI, 1.04-2.47]; RD, 1.7% [95% CrI, 0.1%-4.3%]). All ARB-containing regimens had fewer treatment discontinuations due to AEs than placebo, and these differences were statistically significant for ARB monotherapy (OR, 0.73 [95% CrI, 0.61-0.86]; RD, -0.8% [95% CrI, -1.3% to -0.4%]) and ARBs plus CCBs (OR, 0.61 [95% CrI, 0.47-0.79]; RD, -1.2% [95% CrI, -1.8% to -0.6%]). In network meta-analyses, 5 combination and 2 monotherapy regimens had higher surface under the cumulative ranking curve values than placebo for treatment discontinuation due to AEs, suggesting overall symptomatic improvement compared with placebo. All regimens significantly increased dizziness, and all but CCBs significantly decreased headache compared with placebo.

JAMA retracted the only large trial of ramipril for walking distance in intermittent claudication after its first author admitted data fabrication, and the Journal of Family Practice then retracted its own 2013 commentary on that trial. (Source 25)

• Official position, Certainty not rated.
• Size: not applicable (retraction notice)
• Who: not applicable.
• How long: not applicable.
• Result: the retraction statement records admitted data fabrication after an internal investigation, and that the source article provides no subgroup analysis to determine how much of the reported effect the fabricated data produced.
• Funding: not applicable.

Limit of this finding: The notice quoted here is the Journal of Family Practice withdrawing its own 2013 commentary, "PURLs: ramipril for claudication?", not JAMA’s retraction of the trial. The retraction of the trial itself was issued by JAMA, and this notice reports it. The quoted sentence also carries a small raised 2, a footnote marker whose footnote is not reproduced in the indexed record, so the reference it points to cannot be followed from here. The marker is in the source and has been kept.

According to JAMA's retraction statement, the first author of the article admitted to data fabrication following an internal investigation.

The label records that persistent dry cough has been reported with all ACE inhibitors and always resolves after the drug is stopped. (Source 22)

• Official position, Certainty not rated.
• Size: not stated.
• Who: patients on any ACE inhibitor.
• How long: not stated.
• Result: no rate given in this section; presumed to be caused by inhibition of the degradation of endogenous bradykinin.
• Funding: manufacturer's label (position of the sponsor and FDA, SPL effective 2026-09-18)

persistent nonproductive cough has been reported with all ACE inhibitors, always resolving after discontinuation of therapy

The label sets lower ramipril doses when kidney function is impaired, including a heart-failure ceiling of 2.5 mg twice daily, which is below the 5 mg twice-daily target used when kidney function is normal. (Source 26)

• Official position, Certainty not rated.
• Size: not applicable - regulatory position.
• Who: patients with renal impairment, and patients who are volume depleted or have renal artery stenosis.
• How long: not applicable.
• Result: hypertension with renal impairment: start 1.25 mg once daily, maximum 5 mg total daily; heart failure after myocardial infarction with renal impairment: start 1.25 mg once daily, maximum 2.5 mg twice daily; volume depletion or renal artery stenosis: start 1.25 mg once daily; usual regimens may be followed above an estimated creatinine clearance of 40 mL/min.
• Funding: not stated.

Limit of this finding: Any dose quoted from this label for blood pressure or for heart failure assumes normal kidney function. When the kidneys are impaired the label halves or quarters those doses, and the heart-failure ceiling of 2.5 mg twice daily is lower than the 5 mg twice-daily target quoted elsewhere in this monograph. Doses are set by a prescriber, not by this page.

For patients with heart failure and renal impairment, the recommended initial dose is 1.25 mg ramipril capsules once daily. The dose may be increased to 1.25 mg twice daily, and up to a maximum dose of 2.5 mg twice daily depending on clinical response and tolerability.

What the evidence supports

In the HOPE trial, ramipril 10 mg daily cut the combined rate of heart attack, stroke or cardiovascular death from 17.8% to 14.0% over a mean of five years, and all-cause death from 12.2% to 10.4%. (Source 4)

• Randomized trial, High certainty.
• Size: 9,297 high-risk patients.
• Who: people aged 55 or older with vascular disease or diabetes plus one other cardiovascular risk factor, not known to have a low ejection fraction or heart failure.
• How long: mean of five years.
• Result: primary endpoint 651/4,645 (14.0%) versus 826/4,652 (17.8%), relative risk 0.78, 95% CI 0.70 to 0.86, P<0.001 (absolute reduction 3.8 percentage points, about 1 event prevented per 26 treated over 5 years); cardiovascular death 6.1% versus 8.1%, RR 0.74; myocardial infarction 9.9% versus 12.3%, RR 0.80; stroke 3.4% versus 4.9%, RR 0.68; death from any cause 10.4% versus 12.2%, RR 0.84, P=0.005 (absolute reduction 1.8 percentage points, about 1 death avoided per 56 treated over 5 years)
• Funding: Research Support, Non-U.S. Gov't.

Limit of this finding: The marker "[corrected]" inside this quotation is not part of the journal’s own abstract. It is an indexing note added by the United States National Library of Medicine to flag a published correction, and it appears in the PubMed record this quotation was taken from. It has been kept because the quotation is attributed to that record.

A total of 651 patients who were assigned to receive ramipril (14.0 percent) reached the primary end point, as compared with 826 patients who were assigned to receive placebo (17.8 percent) (relative risk, 0.78; 95 percent confidence interval, 0.70 to 0.86; P<0.001). Treatment with ramipril reduced the rates of death from cardiovascular causes (6.1 percent, as compared with 8.1 percent in the placebo group; relative risk, 0.74; P<0.001), myocardial infarction (9.9 percent vs. 12.3 percent; relative risk, 0.80; P<0.001), stroke (3.4 percent vs. 4.9 percent; relative risk, 0.68; P<0.001), death from any cause (10.4 percent vs. 12.2 percent; relative risk, 0.84; P=0.005), revascularization procedures (16.3 percent vs. 18.8 percent; relative risk, 0.85; P<0.001), cardiac arrest (0.8 percent vs. 1.3 percent; relative risk, 0.62; P=0.02), [corrected] heart failure (9.1 percent vs. 11.6 percent; relative risk, 0.77; P<0.001), and complications related to diabetes (6.4 percent vs. 7.6 percent; relative risk, 0.84; P=0.03).

In the AIRE trial, ramipril started 3 to 10 days after a heart attack in people with clinical heart failure reduced all-cause mortality from 23% to 17%. (Source 5)

• Randomized trial, High certainty.
• Size: 2,006 patients from 144 centres in 14 countries.
• Who: survivors of acute myocardial infarction who had shown clinical evidence of heart failure at any time after the infarct; those with severe resistant heart failure were excluded.
• How long: minimum 6 months, average 15 months.
• Result: 170 deaths (17%) on ramipril versus 222 (23%) on placebo; observed risk reduction 27%, 95% CI 11% to 40%, p = 0.002 (absolute reduction about 6 percentage points, roughly 1 death avoided per 17 treated); risk reduction 19% for the first validated outcome of death, severe or resistant heart failure, myocardial infarction or stroke, 95% CI 5% to 31%, p = 0.008.
• Funding: not stated in the record.

Limit of this finding: This 1993 abstract misspells its own drug, printing "rampiril" for ramipril twice, writes "resistent" for resistant, and prints the confidence interval as "95 % Cl" with a space before the per-cent sign and a lower-case letter L where a capital I is meant. All of that is in the published source and has been kept. The trial also excluded patients with severe heart failure in whom the doctor judged an ACE inhibitor essential, and the 19% figure is for the first of four different events in a patient, not for any one of them.

On intention-to-treat analysis mortality from all causes was significantly lower for patients randomised to receive ramipril (170 deaths; 17%) than for those randomised to receive placebo (222 deaths; 23%). The observed risk reduction was 27% (95 % Cl 11% to 40%; p = 0.002). Analysis of prespecified secondary outcomes revealed a risk reduction of 19% for the first validated outcome (i.e., first event in an individual patient)--namely, death, severe/resistent heart failure, myocardial infarction, or stroke (95% Cl 5% to 31%; p = 0.008). Oral administration of rampiril to patients with clinical evidence of either transient or ongoing heart failure, initiated between the second and ninth day after myocardial infarction, resulted in a substantial reduction in premature death from all causes. This benefit was apparent as early as 30 days and was consistent across a range of subgroups.

The label’s own account of the AIRE trial adds that progression to severe heart failure and heart-failure hospitalisation were also reduced, by 23% and 26%, and that the benefit was seen in both sexes, though older patients may have had a greater benefit than those under 65. (Source 27)

• Official position, Moderate certainty.
• Size: 2,006 patients, 161 centres.
• Who: stable patients 2 to 9 days after acute myocardial infarction with clinical signs of congestive heart failure.
• How long: average 15 months, range 6 to 46 months.
• Result: 27% reduction in risk of death from any cause (p=0.002); progression to severe heart failure reduced 23% (p=0.017); heart-failure-related hospitalisation reduced 26% (p=0.011); benefit seen in both genders and not affected by the timing of initiation, but older patients may have had a greater benefit than those under 65; the label adds that the benefits were seen in patients on and not on aspirin (about 80%), diuretics (about 60%), organic nitrates (about 55%), beta-blockers (about 20%), calcium channel blockers (about 15%) and digoxin (about 12%)
• Funding: manufacturer's label (position of the sponsor and FDA, SPL effective 2026-09-18)

The risks of progression to severe heart failure and of congestive heart failure-related hospitalization were also reduced, by 23% (p=0.017) and 26% (p=0.011), respectively. The benefits of ramipril therapy were seen in both genders, and they were not affected by the exact timing of the initiation of therapy, but older patients may have had a greater benefit than those under 65.

A meta-analysis of 484 placebo-controlled trials found a standard-dose antihypertensive monotherapy lowers systolic pressure by only about 8.7 mmHg, and that doubling the dose adds little. (Source 3)

• Meta-analysis, High certainty.
• Size: 484 trials including 104,176 participants.
• Who: adults in randomised, double-blind, placebo-controlled trials of ACE inhibitors, angiotensin receptor blockers, beta blockers, calcium channel blockers or diuretics; mean age 54, mean baseline blood pressure across the included trials 154/100 mmHg.
• How long: mean follow-up 8.6 weeks.
• Result: monotherapy at standard dose reduced systolic blood pressure by 8.7 mmHg, 95% CI 8.2-9.2, with each doubling of dose adding 1.5 mmHg, 95% CI 1.2-1.7; 45 of 57 standard-dose monotherapies classified as low intensity; dual combinations at one standard dose gave 14.9 mmHg, 95% CI 13.1-16.8.
• Funding: National Health and Medical Research Council, Australia (independent of industry)

Limit of this finding: Two numbers here are easy to misread. The 154/100 mmHg is the average starting blood pressure of the people in the pooled trials, not a threshold at which anything is recommended. And "low intensity" does not mean a low dose or a weak drug: the authors defined low, moderate and high intensity as lowering systolic pressure by under 10, 10 to 19, and 20 mmHg or more, calculated from that same 154 mmHg starting point, so the same drug would be classified differently in people starting lower. The reductions are placebo-corrected and measured over about 8.6 weeks, so they describe blood pressure, not heart attacks or strokes.

On average, monotherapy at standard dose reduced systolic blood pressure by 8·7 mm Hg (95% CI 8·2-9·2), and each doubling in dose conferred an additional 1·5 mm Hg (1·2-1·7) reduction. Dual combinations at one standard dose conferred a 14·9 mm Hg (95% CI 13·1-16·8) reduction in systolic blood pressure, with each doubling of doses of both drugs conferring an additional reduction of 2·5 mm Hg (1·4-3·7). Each 10 mm Hg decrease in baseline systolic blood pressure reduced pressure-lowering efficacy by 1·3 mm Hg (1·0-1·5) for monotherapies, although differences between drug classes were observed. Among 57 monotherapies at standard dose, 45 (79%) were classified as low intensity.

An independent 33-patient randomised trial found ramipril improved treadmill walking distance in intermittent claudication without improving the ankle-brachial index. (Source 7)

• Randomized trial, Very low certainty.
• Size: 33 patients (14 ramipril, 19 placebo); 25 men, mean age 64.6 years.
• Who: patients with intermittent claudication from peripheral arterial disease.
• How long: 24 weeks.
• Result: maximum treadmill walking distance improved by an adjusted mean 131 m, 95% CI 62 to 199, P = 0.001; claudication distance 122 m, 95% CI 56 to 188, P = 0.001; carotid femoral pulse wave velocity -1.47 m/s, 95% CI -2.40 to -0.57, P = 0.002; resting ankle:brachial pressure index not different, 0.02 versus 0.03, P = 0.830; quality of life effect slight and non-significant.
• Funding: Research Support, Non-U.S. Gov't.

Resting ankle : brachial pressure index (ABPI) improved slightly in both ramipril and placebo groups (0.02 (95 per cent c.i. -0.08 to 0.11) versus 0.03 (-0.05 to 0.10); P = 0.830). Ramipril had a slight, non-significant effect on QoL physical domains compared with placebo.

Reducing the risk of heart attack, stroke and cardiovascular death in people aged 55 and over at high cardiovascular risk is an approved indication for ramipril in the United States. (Source 28)

• Official position, Certainty not rated.
• Size: not applicable - regulatory position.
• Who: patients 55 years or older with coronary artery disease, stroke, peripheral vascular disease, or diabetes plus at least one other cardiovascular risk factor.
• How long: not stated in this section.
• Result: no effect size is given in this section; the label cross-refers to its account of the HOPE trial in section 14.2.
• Funding: not stated.

Ramipril capsules are indicated in patients 55 years or older at high risk of developing a major cardiovascular event because of a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes that is accompanied by at least one other cardiovascular risk factor (hypertension, elevated total cholesterol levels, low HDL levels, cigarette smoking, or documented microalbuminuria), to reduce the risk of myocardial infarction, stroke, or death from cardiovascular causes.

Heart failure in the first few days after a heart attack is a second approved indication, and the label states that treating those patients has been shown to lower the risk of death. (Source 29)

• Official position, Certainty not rated.
• Size: not applicable - regulatory position.
• Who: stable patients with clinical signs of congestive heart failure within the first few days after an acute myocardial infarction.
• How long: not stated in this section.
• Result: no effect size is given in this section; the label cross-refers to its account of the AIRE trial in section 14.3.
• Funding: not stated.

Limit of this finding: The label prints this sentence ungrammatically, as "patients have been shown" rather than "patients has been shown". That is the document’s own wording and has been kept.

Administration of ramipril capsules to such patients have been shown to decrease the risk of death (principally cardiovascular death) and to decrease the risks of failure-related hospitalization and progression to severe/resistant heart failure [see Clinical Studies (14.3)].

What the evidence does not support

Ramipril did not significantly reduce the incidence of diabetes or death in people with impaired fasting glucose or impaired glucose tolerance. (Source 6)

• Randomized trial, High certainty.
• Size: 5,269 participants.
• Who: people without cardiovascular disease but with impaired fasting glucose or impaired glucose tolerance.
• How long: median 3 years.
• Result: primary outcome 18.1% on ramipril versus 19.5% on placebo, hazard ratio 0.91, 95% CI 0.81 to 1.03, P=0.15; regression to normoglycaemia more likely on ramipril, hazard ratio 1.16, 95% CI 1.07 to 1.27, P=0.001; 2-hour post-load glucose 135.1 versus 140.5 mg/dL, P=0.01.
• Funding: Research Support, Non-U.S. Gov't.

Limit of this finding: The "primary outcome" in this quotation is a combination of two things, developing diabetes or dying, whichever came first. The definition sits in the part of the paper not quoted here, so the 18.1 per cent and 19.5 per cent figures are not diabetes rates on their own. The trial gave ramipril up to 15 mg a day to 5,269 people for a median of three years alongside a second randomisation to rosiglitazone. It found no significant effect on that combined outcome, and a real but small increase in the chance of blood sugar returning to normal.

The incidence of the primary outcome did not differ significantly between the ramipril group (18.1%) and the placebo group (19.5%; hazard ratio for the ramipril group, 0.91; 95% confidence interval [CI], 0.81 to 1.03; P=0.15). Participants receiving ramipril were more likely to have regression to normoglycemia than those receiving placebo (hazard ratio, 1.16; 95% CI, 1.07 to 1.27; P=0.001).

The same UK routine-care study found no evidence that the difference between an angiotensin receptor blocker and an ACE inhibitor on its main combined cardiovascular outcome varied by ethnicity. (Source 30)

• Cohort study, Low certainty.
• Size: approximately 17,593 Black, 30,805 South Asian and 524,623 White patients.
• Who: patients in England prescribed an ACE inhibitor or an angiotensin receptor blocker between 1 January 2001 and 31 July 2019.
• How long: median follow-up 5.2 years.
• Result: primary composite outcome (cardiovascular death, myocardial infarction, stroke or hospitalisation for heart failure) hazard ratio 0.96, 95% CI 0.95 to 0.98, absolute incidence rate difference -1.01 per 5.5 person-years, 95% CI -1.42 to -0.60; no evidence of heterogeneity by ethnicity on the multiplicative scale (Pint = 0.422) or the additive scale (Pint = 0.287)
• Funding: not stated in the abstract.

Limit of this finding: An interaction P value above 0.05 means this study did not detect a difference between ethnic groups on this outcome. It is not evidence that the groups respond identically, and a study can miss a real difference when the number of events in the smaller groups is low. The heterogeneity the same study did find was on one component of the outcome, death from cardiovascular causes, and is reported separately. This is routine prescribing data, not a randomised trial, so it shows associations rather than effects of the drugs themselves.

We benchmarked results against ONTARGET and observed hazard ratio (HR) 0.96 (95% CI: 0.95, 0.98) for the primary outcome, with an absolute incidence rate difference (IRD)% of -1.01 (95% CI: -1.42, -0.60) per 5.5 person-years. We found no evidence of treatment effect heterogeneity by ethnicity for the primary outcome on the multiplicative (Pint = 0.422) or additive scale (Pint = 0.287).

Where the evidence is mixed

In a UK routine-care study benchmarked against the ONTARGET trial, switching from an ACE inhibitor to an angiotensin receptor blocker avoided more angioedema in Black patients in absolute terms, but was associated with more cardiovascular deaths in that group. (Source 30)

• Cohort study, Low certainty.
• Size: approximately 17,593 Black, 30,805 South Asian and 524,623 White patients.
• Who: patients in England prescribed an ACE inhibitor or an angiotensin receptor blocker between 2001 and 2019, median follow-up 5.2 years.
• How long: median 5.2 years.
• Result: angioedema hazard ratio 0.56, 95% CI 0.46-0.67 for ARB versus ACEi; absolute incidence rate difference -0.49 per 5.5 person-years in Black individuals (number needed to treat 204) against -0.06 in White individuals (number needed to treat 1667); for cardiovascular death ARBs were associated with more events in Black individuals, hazard ratio 1.20, 95% CI 1.02-1.40, number needed to harm 93.
• Funding: not stated in the abstract.

Limit of this finding: Two wording traps in this source, both the authors’. "Absolute risks were higher in Black individuals" is followed by a negative figure: the minus sign means ARBs caused fewer cases of angioedema, and the reduction was larger in Black individuals, not smaller. And the published abstract leaves a bracket unclosed in the South Asian figure. Both have been kept as printed. This is routine-care data, not a trial, so it shows associations; the authors’ warning about UK guidance rests on the cardiovascular-death result quoted here, not on the angioedema result.

However, for cardiovascular-related death, which occurred in 37,554 (6.6%) people, there was strong evidence of heterogeneity on the multiplicative (Pint = 0.002) and additive scale (Pint < 0.001). Compared to ACEi, ARB were associated with more events in Black individuals (HR 1.20 (95% CI: 1.02, 1.40); IRD% 1.07 (95% CI: 0.10, 2.04); number-needed-to-harm (NNH): 93) and associated with fewer events in White individuals (HR 0.91 (95% CI: 0.88, 0.93); IRD% -0.87 (95% CI: -1.10, -0.63); number-needed-to-treat (NNT): 115), and no differences in South Asian individuals (HR 0.97 (95% CI: 0.86, 1.09); IRD% -0.17 (95% CI: -0.87, 0.53)). For angioedema, HR 0.56 (95% CI: 0.46, 0.67) with no heterogeneity for ARB versus ACEi on the multiplicative scale (Pint = 0.306). However, there was heterogeneity on the additive scale (Pint = 0.023). Absolute risks were higher in Black individuals (IRD% -0.49 (95% CI: -0.79, -0.18); NNT: 204) compared with White individuals (IRD% -0.06 (95% CI: -0.09, -0.03); NNT: 1667) and no difference among South Asian individuals (IRD% -0.05 (95% CI: -0.15, 0.05) for ARB versus ACEi.

Where the research disagrees

Whether Black patients should be given an angiotensin receptor blocker instead of an ACE inhibitor because of angioedema risk

• The U.S. ramipril label, SPL effective 2026-09-18, regulatory position citing controlled trials and a post-marketing study: In a large U.S. post-marketing study, angioedema (defined as reports of angio, face, larynx, tongue, or throat edema) was reported in 3/1523 (0.2%) Black patients and in 8/8680 (0.09%) non-Black patients. These rates were not different statistically. (Source 17)
• Baptiste and colleagues, UK routine-care reference-trial emulation, 2024, inverse-probability-weighted cohort of 572,000 patients benchmarked against the ONTARGET trial: These results demonstrate variation in drug effects of ACEi and ARB for some outcomes by ethnicity and suggest the potential for adverse consequences from current UK guideline recommendations for ARB in preference to ACEi for Black individuals. (Source 30)

Whether ramipril improves walking distance in intermittent claudication

• The Journal of Family Practice, retracting its own 2013 commentary after JAMA retracted the trial it discussed, 2016, retraction notice for the journal’s own commentary, following the trial author’s admission of data fabrication: The source article does not provide subgroup analysis to determine how much of an effect the fabricated data may have had on the final reported outcome. (Source 25)
• Shahin and colleagues, independent randomised trial, 2013, double-blind randomised trial, 33 patients, 24 weeks: After 24 weeks, ramipril improved maximum treadmill walking distance by an adjusted mean (95 per cent confidence interval, c.i.) of 131 (62 to 199) m (P = 0·001) (Source 7)

How much

• Reference intake: There is no reference intake for a drug: dosing is set by the prescriber and titrated to blood pressure and tolerance. As a position, the manufacturer's label (SPL effective 2026-09-18) gives a starting dose for hypertension of 2.5 mg once a day in people not on a diuretic, with a usual maintenance range of 2.5 mg to 20 mg per day; for cardiovascular risk reduction it describes a stepped titration from 2.5 mg daily to 10 mg daily; for heart failure after myocardial infarction it starts at 2.5 mg twice daily toward a target of 5 mg twice daily. (Source 31)
• Upper limit: The label's highest stated dose, as a position of the sponsor and FDA (SPL effective 2026-09-18), is 20 mg per day for hypertension, reached as a single dose or two divided doses; the cardiovascular-risk-reduction maintenance dose is 10 mg once daily and the post-infarction heart failure target is 5 mg twice daily. The label also directs that the patient be observed under medical supervision for at least two hours after the first post-infarction dose. (Source 31)
• Studied: HOPE gave ramipril 10 mg orally once daily, or matching placebo, for a mean of five years to 9,297 high-risk patients aged 55 and over. (Source 4)
• Studied: AIRE started ramipril at 2.5 mg twice daily (reduced to 1.25 mg if hypotension occurred) and titrated to a target of 5 mg twice daily, achieved in 77% of those randomised. (Source 27)
• Studied: DREAM gave ramipril up to 15 mg per day, or placebo, for a median of three years to 5,269 people with impaired fasting glucose or impaired glucose tolerance. (Source 6)
• Studied: The independent claudication trial randomised 33 patients to ramipril or placebo for 24 weeks. (Source 7)

A common belief, and what the research shows

The belief: Ramipril is a blood pressure tablet, so if your blood pressure is fine you do not need it, and the cough it causes means something is wrong with your lungs.

What the research shows: Both halves miss the point. The approved indication is not a blood-pressure target at all: ramipril is indicated in people 55 or older at high cardiovascular risk "to reduce the risk of myocardial infarction, stroke, or death from cardiovascular causes", and the label states it "can be used in addition to other needed treatment (such as antihypertensive, anti-platelet, or lipid-lowering therapy)". In HOPE the composite of heart attack, stroke and cardiovascular death fell from 17.8% to 14.0% and death from any cause from 12.2% to 10.4%, so in that population the drug is prescribed for events, not for a number. The cough is not a lung problem at all; the label attributes it to the enzyme ramipril blocks, saying it is "Presumably caused by inhibition of the degradation of endogenous bradykinin", and reports that it is "always resolving after discontinuation of therapy". It is common: in HOPE, cough was a reason for stopping or interrupting treatment in 7% of the ramipril group against 2% on placebo.

Questions and answers

What is it?

Ramipril is a prescription capsule, an angiotensin-converting enzyme inhibitor. It is inactive as swallowed and is converted in the body into ramiprilat, the form that does the work. It is approved for high blood pressure, for reducing heart attack, stroke and cardiovascular death in people aged 55 and over at high risk, and for heart failure after a heart attack. (Source 1)

What does it do in the body?

It blocks the enzyme that makes angiotensin II, the hormone that narrows blood vessels and triggers aldosterone release. Blood vessels relax and pressure falls; less aldosterone means potassium drifts up a little. The same enzyme also destroys bradykinin, and the bradykinin build-up is the presumed cause of the dry cough and of angioedema. (Source 1)

Is it good or bad for you?

For the populations the outcome trials studied, the evidence is about as good as drug evidence gets: HOPE cut death from any cause from 12.2% to 10.4% over five years and AIRE cut it from 23% to 17%. The costs are a cough in roughly one in eight to one in ten, a small risk of angioedema that can be fatal, rising potassium, kidney function that can fall when NSAIDs or dehydration are added, and absolute contraindication in pregnancy. (Source 4)

How do you get more of it?

Ramipril is prescription-only and the dose is chosen and titrated by a prescriber, so this monograph gives no dose for a reader to act on. As a position the label starts hypertension treatment at 2.5 mg once daily with a usual maintenance range of 2.5 mg to 20 mg per day, and notes that if blood pressure is not controlled on ramipril alone a diuretic can be added. (Source 31)

If it is harmful, what reduces it?

If a reaction demands it, the drug is stopped, and for some reactions the label says that immediately: if laryngeal stridor or swelling of the face, tongue or glottis occurs, discontinue ramipril and treat at once. For the common dry cough, the label records that stopping always resolves it. There is no agent that clears ramipril faster. (Source 17)

Why might someone be low in it or missing it?

Nobody is naturally deficient in ramipril. The practical version of this question is why someone stops getting the benefit, and the trial data answer it: in HOPE 34% of the ramipril group discontinued at some point, with cough the leading drug-specific reason, and in the U.S. hypertension trials about 3% stopped for a side effect, cough accounting for 1%. Reduced kidney function and interacting drugs change how much drug effect a given dose produces. (Source 21)

Which whole foods contain it or feed it?

No whole food contains ramipril. Food matters here in the opposite direction, as a source of potassium. Potassium-based salt substitutes are the clearest case: a network meta-analysis of 34 trials in 37,063 people found they lower blood pressure, but the reviewers specifically say kidney disease and hyperkalaemia risk should be ruled out before recommending them, and an ACE inhibitor is itself a potassium-raising drug. (Source 9)

What happens if you do not have it?

For the people the trials enrolled, not taking it means carrying the untreated risk. The placebo arms show what that looked like: in HOPE, 17.8% of the placebo group had a heart attack, stroke or cardiovascular death over five years against 14.0% on ramipril, and 12.2% died of any cause against 10.4%. In AIRE, 23% of the placebo group died against 17% on ramipril. (Source 32)

How can you test for it?

The tests that matter are blood pressure, serum potassium and kidney function, not a ramipril level. The label directs that potassium be monitored in people at risk of hyperkalaemia and when potassium-raising drugs are combined, and that kidney function be monitored periodically in people taking ramipril with an NSAID. These are routine blood tests and are reliable for what they measure. (Source 10)

References

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