Genes and the heart: a quest for new therapeutic strategies. Cambridge Healthtech Institute's First Cardiovascular Genomics Conference. Orlando, FL, USA, 11-12 January 1999.
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Animals↗
Biomedical subjects
A S Hall
Publications and source records attributed to A S Hall.
QT dispersion as a predictor of long-term mortality in patients with acute myocardial infarction and clinical evidence of heart failure.
BACKGROUND: QT interval dispersion is a marker of inhomogeneous ventricular repolarization, and therefore has the potential to predict re-entry arrhythmias. Following acute myocardial infarction, increased QT dispersion has been associated with a higher risk of ventricular arrhythmias. However, whether or not QT dispersion predicts prognosis post-acute myocardial infarction is not clear. We addressed this issue by analysing the AIREX study registry. METHODS: AIREX was a follow-up study of 603 post-acute myocardial infarction patients who exhibited clinical signs of heart failure and were randomly allocated to ramipril or placebo. An interpretable 12-lead ECG obtained between day 0 and day 9 after the index infarction (median time 2 days) was available in 501 patients. We examined whether QT dispersion was a predictor of all-cause mortality in the AIREX study registry (mean follow-up 6 years). RESULTS: QT dispersion measurements were significantly increased in patients who subsequently died (QT dispersion: 92.0 +/- 38.5 ms vs 82.7 +/- 34.3 ins. P=0.005; rate corrected QT dispersion: 105.7 +/- 42.7 ms vs 93.1 +/- 35.9 ms, P<0.001). Univariate analysis showed that QT dispersion as a predictor of all-cause mortality risk (QT dispersion: hazard ratio per l0 ms 1.05, [95% CI 1.02 to 1.09]. P= 0.004; rate corrected QT dispersion: 1-07 [1.03 to 1.10], P<0.001): an increase of 10 ms added a 5-7%, relative risk of death. QT dispersion remained an independent predictor of all-cause mortality risk on multivariate analysis (QT dispersion: 1.05 [1.01 to 1.09], P=0.027; rate corrected QT dispersion: 1.05 [1.01 to 1.09]. P=0.022). CONCLUSION: QT dispersion. measured from Li routine 12-lead ECG following acute myocardial infarction complicated by heart failure provides independent information regarding the probability of long-term survival. However. the low sensitivity of this electrocardiographic marker limits its usefulness for risk stratification if used in isolation.
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beta blocker treatment and other prognostic variables in patients with clinical evidence of heart failure after acute myocardial infarction: evidence from the AIRE study.
OBJECTIVES: To examine clinical outcomes associated with optional beta blockade in a population of patients with evidence of heart failure after myocardial infarction. DESIGN AND PATIENTS: Data from the acute infarction ramipril efficacy (AIRE) study were analysed retrospectively. At baseline 22.3% of the patients were receiving a beta blocker. To minimise confounding, beta blocker and diuretic treatments, presence of clinical signs of heart failure, left ventricular ejection fraction, and 16 other baseline clinical variables were simultaneously entered in a multivariate Cox regression model. In addition, the same analysis was repeated separately within a high and a low risk group of patients, as defined according to the need for diuretic treatment. RESULTS: beta Blocker treatment was an independent predictor of reduced risk of total mortality (hazard ratio 0.66, 95% confidence interval (CI) 0. 48 to 0.90) and progression to severe heart failure (0.58, 95% CI 0.40 to 0.83) for the entire study population. There were similar findings in high risk patients requiring diuretics (0.59, 95% CI 0.40 to 0.86; and 0.58, 95% CI 0.38 to 0.89). CONCLUSIONS: beta Blocker treatment is associated with improved outcomes in patients with clinical evidence of mild to moderate heart failure after myocardial infarction. Most importantly, high risk patients with persistent heart failure appear to benefit at least as much as lower risk patients with transient heart failure.
Adrenergic beta-Antagonists↗
Family therapy with intellectually and creatively gifted children.
Few family therapists have expertise in the psychology of giftedness, and little research has been conducted to determine the effectiveness of family therapy with talented children and their families. The purposes of this paper are: (1) to provide family therapists with information on the unique psychosocial stressors associated with giftedness and (2) to stimulate further research and development on the efficacy of family therapy in alleviating distress and actualizing potential in gifted and talented children and their families. The paper provides a critical overview of the existing research literature on gifted children and their families. First, current conceptualizations of giftedness are described. Then the research literature on the characteristics of intellectually and creatively gifted children and their families is reviewed with an emphasis on the endogenous (individual) and exogenous (systemic) factors that can create or exacerbate psychosocial problems. Finally, we suggest an eclectic, eco-systemic approach to three common concerns that bring gifted children and their families to therapy.
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Structure and in vitro function of human subcutaneous small arteries in mild heart failure.
The structure and function of subcutaneous small arteries from patients with mild heart failure (n = 27) 6-43 mo after myocardial infarction were compared with vessels from healthy control subjects (n = 10). Patients were randomized to treatment with placebo or the angiotensin-converting enzyme inhibitor ramipril starting 3-10 days after myocardial infarction. Dissected arterial vessels were mounted on a wire myograph for measurement of morphology and isometric tension. Morphology was not different in arteries from the three groups. Responses to norepinephrine, angiotensin II, and electrical field stimulation were similar in arteries from placebo-treated patients with mild heart failure and control subjects. Similarly, endothelium-dependent and -independent relaxation was normal in arteries from patients with mild heart failure. Ramipril therapy was associated with functional alterations: vasoconstrictor responses to norepinephrine and angiotensin II were significantly enhanced compared with placebo (P < 0.001). These data suggest that vascular structure and function are not different in vitro in subcutaneous arteries from placebo-treated patients with mild heart failure. Angiotensin-converting enzyme inhibitor therapy is associated with enhanced vasoconstriction to norepinephrine and angiotensin II, which may reflect upregulation of receptor-mediated events.
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Follow-up study of patients randomly allocated ramipril or placebo for heart failure after acute myocardial infarction: AIRE Extension (AIREX) Study. Acute Infarction Ramipril Efficacy.
BACKGROUND: In the Acute Infarction Ramipril Efficacy (AIRE) Study, the effect of angiotensin-converting-enzyme (ACE) inhibition on the survival of patients with clinical heart failure after acute myocardial infarction (AMI), was assessed. At an average follow-up time of 15 months after randomisation, all-cause mortality was reduced from 22.6% (placebo group) to 16.9% (ramipril group) representing an absolute mortality reduction of 5.7% and a relative risk reduction of 27% (95% CI 11-40%; p = 0.002). Our aim in this study was to assess the long-term (3 years after the AIRE Study closed) magnitude, duration, and reliability of the survival benefits observed after treatment with ramipril (target dose 5 mg twice a day) when compared with placebo. METHODS: We investigated the mortality status of all 603 patients recruited from the 30 UK centres involved in the AIRE Study. Through government records we were able to confirm the death or survival of all 603 patients exactly 3 years after the close of the AIRE Study. Follow-up was for a minimum of 42 months and a mean of 59 months. The average duration of treatment with masked trial medication was 13.4 months for placebo and 12.4 months for ramipril. FINDINGS: By 0000 h March 1, 1996, death from all causes had occurred in 117 (38.9%) of 301 patients randomly assigned placebo and 83 (27.5%) of 302 patients randomly assigned ramipril, representing a relative risk reduction of 36% (95% CI 15-52%; p = 0.002) and an absolute reduction in mortality of 11.4% (114 additional 5-year survivors per 1000 patients treated for an average of 12.4 months). INTERPRETATION: Our data provide robust evidence that administration of ramipril to patients with clinically defined heart failure after AMI results in a survival benefit that is not only large in magnitude, but also sustained over many years.
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Reactivity-based coronary vasospasm independent of atherosclerosis in rhesus monkeys.
OBJECTIVES: We studied the hypothesis that in the absence of vascular pathology, coronary artery vasospasm occurs as a result of local regions of vascular muscle hyperreactivity. We aimed to explore the basis for a functional etiology of those vasospasms not explained on a structural basis. BACKGROUND: Ovariectomized rhesus monkeys (Macaca mulatta) without injury or significant vascular disease were stimulated with platelet release products, and angiograms were compared with those from vasospasms induced in human patients. METHODS: We used intracoronary (IC) injections of serotonin, thromboxane A2 (U46619), endothelin 1 or angiotensin II in concentrations 3 to 10 times that which reduced coronary artery diameter by 50%. RESULTS: Although no agent alone caused vasospasm, the combination of pathophysiologic concentrations of serotonin and the stable thromboxane A2 mimetic, U46619, injected through an IC catheter, synergistically caused coronary vasospasm on the second or third challenge in five of seven monkeys. These drug-induced vasospasms were similar to vasospasms induced by mechanical injury followed by serotonin, and to those stimulated in human IC diagnostic tests, as judged by onset, appearance, kinetics and vasodilator reversal. CONCLUSIONS: These studies in ovariectomized monkeys revealed that coronary vasospasm can be stimulated without preexisting vascular pathology, endothelial denudation or injury. Reproducible vasospasm of primate coronary arteries in response to these two endogenous pathophysiologic vasoconstrictors, which are thought to be precipitating stimuli in the etiology of vasospasm, suggests that structure-independent epicardial vasospasm can be an important element in serious cardiac ischemic events, particularly the focal, persistent vasospasms that occur without plaques or injury.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Do ACE inhibitors provide protection for the heart in the clinical setting of acute myocardial infarction?
Large randomised clinical trials have shown ACE inhibitors to improve survival after acute myocardial infarction (AMI). The precise mechanism underlying this benefit is not fully established, despite extensive research. There is also controversy with regard to the clinical use of these drugs, particularly the need for selection of patients prior to treatment and the timing of drug initiation and withdrawal for maximum benefit. Animal models of AMI used to assess drug effects are of limited value in understanding the mechanisms of benefit because they involve significantly different pathophysiology from that which occurs in humans. Here we propose that the benefit of ACE inhibitor therapy is largely confined, post-AMI, to those with evidence of left ventricular dysfunction clinically or on investigation, and suggest the continuing importance of treatment distant from the acute event. We argue that the beneficial effects are, at least in part, related to a reduction in the direct toxic effects of angiotensin II and catecholamines on cardiomyocytes resulting from the long term excess stimulation of the renin-angiotensin and sympathetic systems in these patients. Importantly, we believe that for some patients after AMI there is little or no benefit to be gained from treatment and that, in fact, careful analysis of the trials suggests that ACE inhibitors may be associated with adverse outcomes in some individuals. Finally, since ACE inhibitors also potentiate bradykinin and other peptides, their beneficial action may not simply be due to reducing the formation of angiotensin II. The proportion of the benefit that may be via bradykinin is difficult to assess, especially in humans. However, the advent of the angiotensin receptor antagonists has provided the opportunity to investigate this important issue.
Angiotensin II↗
Effect of ramipril on morbidity and mode of death among survivors of acute myocardial infarction with clinical evidence of heart failure. A report from the AIRE Study Investigators.
BACKGROUND: The importance of the effects of ACE inhibitors on sudden death, progressive heart failure and recurrent infarction to the reduction in overall mortality in heart failure and after myocardial infarction is disputed. METHODS: The AIRE study randomized 2006 patients with clinical or radiological evidence of heart failure within 2-9 days of a myocardial infarction to receive ramipiril 5 mg b.d. or matching placebo. Outcomes were assessed independently by members of an end-points committee blinded to treatment allocation. RESULTS: Fewer patients developed severe resistant heart failure as their first validated end-point on rampril, despite the greater number of at-risk survivors, compared to placebo (n = 143 vs 178; risk reduction 23%; CI 5 to 39%; P = 0.017). Ramipril did not alter the rate of reinfarction or stroke. Irrespective of treatment allocation 182 (46%) patients developed resistant heart failure prior to death. A validated acute or remote myocardial reinfarction occurred in 76 (19%) patients prior to death and chest pain occurred in 90 (23%) patients around the time of death suggesting an ischaemic element to these deaths Eighty deaths occurred on the index admission, 167 during re-admission and 145 out-of-hospital. Sudden death accounted for 54% of all deaths and 93% of out-of-hospital deaths. Ramipril reduced the risk of sudden death by 30% (95% CI: 8-47%; P = 0.011). However, overall, 45% of those patients who died suddenly had severe or worsening heart failure prior to their death. Only 39% of sudden deaths were considered to be due to arrhythmias. Ramipril reduced the risk of death from circulatory failure by 18%, but this did not reach statistical significance (95% CI; 41 to -14%; P = 0.237). The magnitude of the effects on sudden death and death due to circulatory failure were not significantly different. However, 38% of the reduction in overall mortality was from the subgroup with sudden death who had developed prior severe resistant heart failure (placebo n = 35, ramipril n = 15), again emphasizing the marked benefit in preventing failure. Ramipril did not selectively alter the proportion of in- to out-of-hospital deaths. CONCLUSION: Ramipril reduces mortality and progression to resistant heart failure among patients with evidence of heart failure early after myocardial infarction. Retarding the progression of heart failure appears to be a major factor contributing to the reduction in mortality both by reducing circulatory failure and by reducing sudden death.
Adult↗
Increasing prescription of drugs for secondary prevention of myocardial infarction. Authors' recommendations are too restrictive.
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Adrenergic beta-Antagonists↗
High resolution magnetic resonance imaging of the anal sphincter using a dedicated endoanal coil. Comparison of magnetic resonance imaging with surgical findings.
PURPOSE: To obtain high resolution images of the anal sphincter and adjacent anorectum using an endoanal coil in patients with sepsis, trauma, and low rectal tumors and to compare imaging appearances with findings at time of surgery. PATIENTS AND METHODS: A cylindrical saddle geometry coil (diameter, 9 mm; length, 75 mm) was used to examine 30 patients (mean age, 53.6 years). Pathologies included perianal sepsis (10 patients), obstetric trauma (7 patients), and low rectal tumors (13 patients). Imaging was performed on an 0.5-T Picker Asset or 1.0-T Picker HPQ Vista (Picker International, Highland Heights, OH). T1 and T2 weighted and short inversion time inversion recovery transverse images and T1 weighted coronal images were obtained. Intravenous gadopentetate dimeglumine (0.1 mmol/kg) was given to all patients with suspected infection and neoplasms. RESULTS: Abscesses and fistulas identified using magnetic resonance imaging (MRI) in patients with perianal sepsis were confirmed at surgery in all cases; site of fistulous internal opening into the anal canal was correctly identified in 80 percent of cases. Extent of sphincter tear was correctly assessed on endoanal MRI in all patients with obstetric trauma when compared with surgical findings. Tumor invasion of anal sphincter was seen in 38.5 percent of low rectal carcinomas. CONCLUSIONS: MRI with an endoanal coil provides detailed images of the site and extent of anal fistulas, sphincter tears, and local tumors and is of considerable value in preoperative assessment.
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How ACE inhibitors reduce death from myocardial infarction: hypotheses from the AIRE study. Acute Infarction Ramipril Efficacy study.
Doctors treat patients, not populations. 'Evidence-based' practice is essential but extrapolation to the individual patient is always necessary and this fact is well illustrated by data from trials of ACE inhibitors post-myocardial infarction. In the AIRE (Acute Infarction Ramipril Efficacy) study, 2,006 patients with some evidence of heart failure, even if transient, after a myocardial infarction, were randomised to receive oral ramipril or placebo in addition to standard treatment. Follow-up was for a minimum of six and an average of 15 months. The risk reduction in total mortality was 27% (95% CI 11-40%; p = 0.002); approximately 40 lives might be expected to be saved for every 1000 patients treated for one year. Benefit was apparent within weeks of starting treatment. Additional data from the AIRE study are considered in relation to the findings of other mortality trials. It is argued that ACE inhibitors offer most to those patients with impaired left ventricular function through a mechanism not related to the prevention of myocardial re-infarction.
Angiotensin-Converting Enzyme Inhibitors↗
Mode of death in chronic heart failure. A request and proposition for more accurate classification.
The proportion of patients reported to die suddenly or from progressive circulatory failure is not consistent among studies of heart failure. Lack of an adequate or consistent classification of how patients die contributes to the current confusion over the mode of death in heart failure. Defining how patients with heart failure die could be important in developing strategies to reduce the continuing high mortality associated with this condition. We identified 27 studies that reported 50 or more deaths among patients with heart failure to ascertain how death was classified. Definitions of sudden death appeared heterogeneous and the majority of studies failed to publish or make reference to how circulatory failure was defined. A framework for the classification of the mode of death has been developed in which clear separation of the activity and place at the time of death, cause of death, mode of death, and events prior to death is made (ACME: Activity, Cause, Mode and Event). This mode of classifying death has been successfully piloted in two mortality studies; AIRE and NETWORK. Classifying mortality in this way will help identify pathways leading to death and hence suggest therapies and strategies to reduce mortality in patients with heart failure, a group of patients whose prognosis remains poor.
Adult↗
Inhibition of the renin-angiotensin system after acute myocardial infarction--treat first, select later?
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Angiotensin-Converting Enzyme Inhibitors↗
Laser ablation of the endometrium: MR appearance during and after treatment and the relation of MR appearance to clinical outcome.
OBJECTIVE: Our objective was to study the appearance of the uterus on MR images obtained during and 3 months after laser ablation of the endometrium and to determine if a correlation exists between the MR imaging findings and the subsequent clinical outcome. The appearance could then be used to guide the application of laser energy during the procedure to optimize the clinical result. SUBJECTS AND METHODS: Eight women 34-55 years old (mean, 42 years old) with symptoms of heavy, painful menses underwent laser ablation under epidural anesthesia. Imaging was done on a 0.5-T Picker Asset system with a pelvic phased-array receiver coil using conventional T1-weighted spin-echo, T2-weighted spin-echo, and gradient-recalled-echo sequences. Images were obtained preoperatively, after ablation of the anterior surface, after completion of the procedure, and 3 months later. Images were visually assessed for signal intensity changes in the endometrium and myometrium by two observers in conference. Images were quantitatively analyzed by measuring uterine volume and the width of the endometrium, junctional zone (JZ), and outer myometrium (OM) on the T2-weighted images. Preoperative and 3-month postoperative symptom scores including duration, amount of bleeding, and associated pain were recorded. RESULTS: MR images obtained immediately after treatment showed an increase in the volume of the uterus (mean, 21%). Endometrial thickness increased in five patients, and the JZ:OM ratio increased on the T2-weighted scans in six patients. The increase in the ratio probably represented myometrial edema. Two patients with persistent symptoms were treated with hysterectomy 6 weeks postoperatively. Of the remaining six patients, five showed an improvement in symptom scores after 3 months. The uterus returned to its preoperative size after 3 months in three patients, endometrial thinning was noted in two, and the JZ:OM ratio remained increased in two. The difference between the mean improvement in symptom scores at 3 months was significant in the patients with and without the endometrial swelling seen immediately after treatment. No statistically significant correlation existed between the amount of perioperative uterine swelling or the increase in JZ:OM ratio and the improvement in symptom scores at 3 months. CONCLUSION: On laser ablation of the endometrium, MR imaging showed significant immediate uterine swelling as well as an increase in the endometrial thickness and JZ:OM ratio. The presence of immediate endometrial swelling and the reduction in the JZ:OM ratio after 3 months correlated with a subsequent improvement in symptom scores. Perioperative endometrial swelling rather than myometrial changes is therefore an indicator of clinical outcome.
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Who should be treated with angiotensin-converting enzyme inhibitors after myocardial infarction?
Angiotensin-converting enzyme (ACE) inhibitors are now established drugs in the treatment of hypertension and heart failure. However, their use in patients after a myocardial infarction has occurred remains controversial. The major clinical question regarding ACE inhibitors is whether they should be given to all patients immediately after thrombolysis or whether their use should be restricted to a particular subgroup. This question has now been addressed in several large-scale trials of mortality after myocardial infarction, and no important new information seems likely to emerge on the issue. Clinicians must therefore decide what their practice will be on the basis of data that are currently available. The authors of the recently published Gruppo italiano per lo Studio delta Sopravvlvenza nell' infarcto Miocardico (GISSI-3) and Fourth International Study of Infarct Survival (ISIS-4) mega-trials advocate a policy of widespread and early use of ACE inhibitors in all patients after myocardial infarction occurs. However, the small mortality benefit observed from use of ACE inhibitors in these studies lacks certainly and may prove difficult to reproduce in the general population of patients who have had an infarct outside the setting of a trial. Although patients were essentially not selected apart from the exclusion of those with marked hypotension, the low 6-month and 1-year mortality figures indicate "selection" compared with the typical population of patients who have had a myocardial infarction. Furthermore, a significant long-term mortality benefit was not observed with the short-term (4- to 6-week) use of ACE inhibitors in these trials. In contrast, in the Survival and Ventricular Enlargement (SAVE), Acute Infarction Ramipril Efficacy (AIRE), and Trandopril Cardiac Evaluation (TRACE) trials, where evidence of impairment of ventricular function was used to select patients, both a marked and certain benefit regarding mortality was apparent from long-term prescription of these drugs. Importantly, the marked benefit observed in these selected patients may have been "diluted out" in the larger scale trials of unselected patients where the majority may have gained little and some may have been harmed by treatment or its withdrawal. In most of the large mortality trials the rationale for use of ACE inhibitors after myocardial infarction was stated to be their likely beneficial effect on "remodeling" of the heart after "Infarct expansion." Because adverse remodeling occurs in only a proportion of patients after a heart attack, the benefits of ACE inhibitor therapy might be predicted to be largely limited to this group, which would favor a selective policy. However, strong claims have been made that ACE inhibitors have other important actions, including prevention of myocardial infarction. If this is confirmed in a number of ongoing large-scale trials. then an even ore widespread use of these agents can be expected.
Angiotensin-Converting Enzyme Inhibitors↗
What have the ACE-inhibitor trials in postmyocardial patients with left ventricular dysfunction taught us?
A series of elegant experimental studies and careful clinical observation over a decade or more have led to the concept of 'infarct expansion' and 'remodelling' of the heart, culminating in a number of major mortality studies indicating the effectiveness of angiotensin-converting enzyme (ACE) inhibitors in patients after myocardial infarction (MI). But has this concept been too narrow in predicting which patients might benefit from treatment with ACE inhibitors? Measurable infarct-expansion with progressive dilatation probably occurs in less than 20% of patients, whereas increase in volume and hypertrophy of the heart as responses to compromised function are likely wherever significant myocardial damage has occurred. Irrespective of infarct expansion, cumulative extensive damage can lead to an inevitable downward spiral with gross ventricular dilatation and death in heart failure. But in the majority of patients after MI a 'new equilibrium' is established in which initial dilatation and subsequently hypertrophy restore adequate function. Is it possible to distinguish patients in whom the cost and inconvenience of long-term therapy with an ACE inhibitor justify the likely benefit from treatment after an MI? The SAVE, AIRE and recent TRACE studies allow a rational approach for the clinician, indicating the effectiveness of these drugs in patients with evidence of impaired ventricular function. However, the prospect that ACE inhibitors prescribed long term might also prevent myocardial reinfarction could justify wider use. Post-MI patients are an easily identifiable high-risk group for a cost-effective programme of secondary prevention. Reinfarction in an already damaged ventricle carries a particularly poor prognosis and its prevention by ACE inhibitors could make a major contribution to the undoubted benefit from these agents. The recently completed TRACE study with its long-term follow-up may help resolve this issue, which is also being investigated in a number of long-term prospective studies in populations at high risk of cardiovascular disease.
Angiotensin-Converting Enzyme Inhibitors↗
Angiotensin-converting enzyme inhibitors after myocardial infarction: indications and timing.
A number of major studies have examined the impact of angiotensin-converting enzyme inhibitors on mortality in patients with ischemic heart disease. However, in these studies, selection of patients, choice of agent and timing of treatment after myocardial infarction have differed. In the Second Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS II), all patients, unless hypotensive, were treated immediately after thrombolysis with placebo or intravenous enalaprilat followed by oral therapy. In contrast, in the Survival and Ventricular Enlargement (SAVE) study, patients were selected with a reduced radionuclide ejection fraction and without overt ongoing ischemia. Despite these different approaches, both studies were based on the rationale that angiotensin-converting enzyme inhibition would beneficially affect infarct expansion and subsequent remodeling. The SAVE study reported a significant reduction in mortality rate (19% risk reduction, 95% confidence interval [CI] 3% to 32%) over an average follow-up period of 42 months, but with no observable impact on mortality rate until almost 1 year into treatment. The CONSENSUS II trial closed prematurely, with no benefit (a 10% increase in risk, 95% CI 7% reduction to 29% increase) apparent from enalapril after 6 months of follow-up. The recently reported but unpublished findings of Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI-3) and the Fourth International Study of Infarct Survival (ISIS-4) indicate a small benefit from early (within 24 h) short-term (4 to 6 weeks) treatment of all patients, unless hypotensive, after a myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin-Converting Enzyme Inhibitors↗