Large dose sublingual nitroglycerin in acute myocardial infarction: Relief of chest pain and reduction of Q wave evolution

Thirty patients with acute myocardial infarction admitted 2.1 ± 1.1 (mean ± standard deviation) hours after the onset of pain and with S-T segment elevation in multiple leads in the standard electrocardiogram were given either intravenous morphine (15 patients) or sublingual nitroglycerin (15 patients), and the effect on pain and QRS changes was observed. Nitroglycerin was administered repetitively in large doses while systolic blood pressure was maintained above 100 mm Hg. Chest pain failed to respond within 30 minutes In two patients who received nitroglycerin. In the remaining 13 patients nitroglycerin produced partial relief of pain in 17 ± 5 minutes and complete relief in 127 ± 65 minutes, requiring a cumulative dosage of 23.7 ± 38.7 mg in 16 ± 7 divided doses. An average of 14.9 ± 7.1 mg of morphine in 3.3 ±1.5 divided doses produced complete relief of pain in a similar period (134 ± 77 minutes [difference not significant]). In patients receiving morphine, Q waves developed at 24 and 48 hours, respectively, in 62 (72 percent) and 66 (77 percent) of a total of 86 sites with initial S-T segment elevation in the standard 12 lead electrocardiogram. In nitroglycerin responders, Q waves developed at 24 and 48 hours, respectively, in only 21 (28 percent, p < 0.001) and 22 (29 percent, p < 0.001) of the 76 sites with initial S-T segment elevation. Other electrocardiographic estimates of the extent of myocardial necrosis, including the percent reduction in R wave amplitude and the relative changes in R and Q wave amplitude, also were significantly less in those receiving nitroglycerin. There was no in-hospital mortality. Thus, large and frequent doses of nitroglycerin when used in the hyperacute phase of acute myocardial infarction can effectively abolish chest pain and limit later electrocardiographic signs of myocardial necrosis.     

Effectiveness of intravenous administration of nicorandil in a patient with variant angina refractory to continuous intravenous nitroglycerin

Variant angina usually responds to conventional treatment with nitrates and calcium antagonists. However, severe variant angina refractory to intensive anti-anginal treatment can be catastrophic because prolonged occlusion of a major coronary artery can result in myocardial infarction, severe cardiac arrhythmia, and sudden death. We report a patient with active variant angina which was refractory to conventional treatment including sublingual nitroglycerin and intravenous nitroglycerin administration. Only intravenous administration of nicorandil was consistently effective in eliminating chest pain of the patient.     

Usefulness of massive oral nicorandil in a patient with variant angina refractory to conventional treatment

A 67-year-old man, who was previously diagnosed with vasospastic angina and treated with standard therapy, was admitted to our hospital because of recurrent chest pain refractory to sublingual nitroglycerin. Admission electrocardiography revealed ST segment elevation in II, III and aV(F), and his symptoms were relieved by intravenous bolus administration of nicorandil. He was diagnosed to have active variant angina, and remained symptomatic even after treatment with calcium antagonists and nitrates at optimal doses. Intravenous bolus administration of nicorandil was consistently effective to relieve his symptoms. Anginal attack was finally prevented by massive oral nicorandil in addition to conventional treatment.     

Intravenous isosorbide dinitrate infusion in the management of unstable angina pectoris refractory to conventional medical therapy

During the past 2 years, 102 patients were treated for unstable angina pectoris (AP) in our department. Fifteen of them had recurrent chest pain at rest despite treatment with various anti-anginal agents, or prolonged chest pain unresponsive to sublingual nitroglycerin; they received intravenous isosorbide dinitrate (ISDN) infusion. A rapid bolus injection of 2 to 6 mg followed by an infusion of 2 to 5 mg/hr was given to 10 patients with acute chest pain, and 5 patients, who were free of chest pain at the time, but had repeated episodes of angina in the past 24 hours, were given ISDN infusion without a bolus injection. Chest pain disappeared completely in 13 patients, but recurred in 2 of them when the dose was tapered. Two other patients experienced recurrent chest pain during ISDN infusion, and additional boluses were given. The hospital course was uneventful in 11 patients. Four patients who had recurrent anginal attacks underwent emergency coronary cineangiography under intraaortic ballon counterpulsation and aorto-coronary bypass surgery. There were no hospital deaths, no one had subsequent acute myocardial infarctions, and only 2 patients had mild to moderate headache as a side effect. Although the patient population is small, intravenous ISDN infusion is useful in the management of severe unstable AP.     

Refractory ergonovine-induced coronary vasospasm: Importance of intracoronary nitroglycerin

Recent experience has suggested that the ergonovine maleate test is a safe procedure for the diagnosis of variant angina pectoris, because ergonovine-induced coronary vasospasm has generally been reversible by sublingual nitroglycerin. This report describes five cases of ergonovine-induced coronary vasospasm that were refractory to sublingual nitroglycerin. Four of these patients had cardiac arrest. In two patients the vasospasm was responsive to intracoronary nitroglycerin administration. Three patients died as a result of the test. The two survivors differed from the nonsurvivors in the total dose of ergonovine given (0.1 and 0.15 mg versus 0.17, 0.3 and 0.3 mg, respectively) and in the method of administration of ergonovine. The survivors were given serial doses of 0.05 mg each, whereas the three nonsurvivors received either larger initial doses (0.1 followed by 0.07 mg) or progressive incremental doses (0.05, 0.1 and 0.15 mg serially). Sublingual nitroglycerin, given to all five patients, and intravenous nitroglycerin, given to three of the five, were ineffective in reversing vasospasm. Intracoronary nitroglycerin favorably altered the course of the survivors. Thus, the ergonovine maleate test is not benign and may cause severe coronary vasospasm that is unresponsive to sublingual and intravenous nitroglycerin, but may be reversed by intracoronary nitroglycerin.     

Sublingual administration of captopril in patients with acute myocardial ischemia.

To investigate the anti-ischemic capability of the angiotensin-converting enzyme inhibitor captopril, 10 patients with acute myocardial ischemia (angina pectoris less than 1 h, ST-segment depression greater than or equal to 0.1 mV, no rise in creatine phosphokinase) received 25 mg captopril sublingually after being treated with an intravenous infusion of nitroglycerin (3 mg/h) and heparin (1200 IU/h) for 1 hour. A control group of 10 patients received placebo instead of captopril. Results showed a decrease of the initial ST-segment depression from 0.25 +/- 0.04 to 0.2 +/- 0.03 mV (p less than 0.01) with nitroglycerin for the captopril group and from 0.26 +/- 0.05 to 0.21 +/- 0.05 mV (p less than 0.01) for the control group. An additional decrease to 0.13 +/- 0.03 mV (p less than 0.001) was measured after sublingual captopril, while no significant change was found in the placebo group (0.19 +/- 0.04 mV). In both groups, 3 patients had no incidents of angina after 1-h nitroglycerin infusion. An additional 6 patients resolved their complaints after captopril administration in contrast to only 1 after placebo. Two patients in the placebo group required increased doses of nitroglycerin because of impairment of anginal complaints. Hemodynamic measurements documented a significant drop of pulmonary vascular resistance after a 1-h infusion of nitroglycerin (-12.9% and -13.1%, respectively, p less than 0.05), while all other parameters remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary arterial spasm and Prinzmetal's variant form of angina induced by hyperventilation and Tris-buffer infusion.

Vigorous hyperventilation was induced for five minutes immediately after a five-minute infusion of 100 ml of Tris-buffer (pH 10) in nine patients with Prinzmetal's variant angina. In eight of the patients, chest pain with ischemic changes in the electrocardiogram occurred during this procedure or within five minutes after it ended. Coronary arterial spasm appeared after the procedure and disappeared after the administration of nitroglycerin in all four patients in whom coronary cinearteriography was performed. This was evident both before and after the procedure and after sublingual administration of nitroglycerin (0.6 mg). The oral administration of 90 mg of diltiazem, a calcium antagonistic drug, two hours before, completely suppressed the attack induced by the procedure in all of the five patients who received this drug. We conclude that hyperventilation plus Tris-buffer infusion induces coronary arterial spasm and anginal attack in patients with Prinzmetal's variant angina and that diltiazem suppresses these reactions.     

Rebound myocardial ischaemia following abrupt interruption of intravenous nitroglycerin infusion in patients with unstable angina at rest

Isolated observations prompted a prospective study of the possible occurrence of myocardial ischaemia following abrupt discontinuation of intravenous infusion of nitroglycerin in 46 consecutive patients with unstable angina. In 26 (55%, group 1), but not the remainder (45%, group 2), cessation of nitroglycerin produced in 10.3 +/- 5.8 (mean +/- SD) minutes ECG changes comparable with those of spontaneous angina without significant changes in heart rate and blood pressure. Reproducible results were observed in 18/20 patients in whom the test was repeated. In four patients with two positive tests, a third test failed to elicit ischaemia 15 min after sublingual administration of 5 mg isosorbide dinitrate. An ergonovine test performed in four other patients with a positive test produced similar ECG changes. Thus, acute interruption of intravenous nitroglycerin infusion in patients with unstable angina is often associated with acute myocardial ischaemia. The lack of preceding changes in heart rate and blood pressure and the similarities with the spontaneous episodes and with those produced by ergonovine, strongly suggest a rebound coronary vasoconstrictive phenomenon as the underlying mechanism.     

Importance of maintaining systemic blood pressure during nitroglycerin administration for reducing ischemic injury in patients with coronary disease. Effects on coronary blood flow, myocardial energetics and left ventricular function.

Because of the controversy concerning the effects on myocardial ischemia of maintaining systemic pressure concomitant with administration of nitroglycerin, this study was undertaken of the actions of nitroglycerin, with and without simultaneous phenylephrine infusion, on coronary blood flow, myocardial energetics and left ventricular function in 17 patients with multivessel coronary artery disease. Five minutes after sublingual administration of 0.4 mg of nitroglycerin, mean arterial pressure, left ventricular filling pressure, cardiac index and coronary sinus blood flow were reduced (P < 0.05) from control values. With mean arterial pressure raised to control level with phenylephrine in 10 patients (Group I), values for coronary sinus blood flow, myocardial perfusion gradient, cardiac efficiency index and ratio of coronary sinus flow/cardiac output all increased (P < 0.05) compared with values in 7 patients receiving only nitroglycerin (Group II) and in patients receiving nitroglycerin before phenylephrine in Group I and with the values in 7 patients who received no phenylephrine. Left ventricular function and coronary vascular resistance were unchanged (P > 0.05) from control values by the addition of phenylephrine to nitroglycerin. Because myocardial oxygen extraction decreased while coronary sinus flow increased, the phenylephrine-induced increase in coronary flow was not due to augmented cardiac oxygen demands. Thus, preservation of systemic pressure concomitant with nitroglycerin enhances myocardial perfusion. From these findings, with greater nitroglycerininduced decreases in mean arterial pressure and coronary flow in patients with acute ischemia, it appears that phenylephrine with nitroglycerin may particularly improve myocardial energetics.     

Nitroglycerin infusion after percutaneous coronary intervention does not influence short- and long-term outcome--a prospective NAPI (Nitroglycerin Administration after Percutaneous Intervention) study

BACKGROUND: Although the benefit of nitroglycerin infusion in patients after elective coronary angioplasty has not been established, this regimen is routinely used in some centres. AIM: The Nitroglycerin Administration after Percutaneous Intervention (NAPI) study tested the efficacy of routine nitroglycerin infusion on the 1st day after percutaneous coronary intervention (PCI) in a double-blind randomised single-centre clinical trial. METHODS: We randomly assigned 200 patients scheduled for elective PCI to treatment with nitroglycerin (100 patients, age 58+/-6 years, infusion up to 100 microg/min) or placebo (100 patients, age 57+/-5 years, p=NS, NaCl 0.9%) for 12 hours after PCI. Patients with acute myocardial infarction, haemodynamic instability during PCI and known intolerance to nitrates were excluded. Patients who were randomised to the placebo group had the possibility to receive nitroglycerin infusion according to the attending physician's decision. Clinical endpoints (cardiac death, myocardial infarction, postprocedural chest pain, unstable angina and repeated PCI) were assessed in hospital and out of hospital with follow-up extended to 24 months. RESULTS: There were no differences during in-hospital stay between those receiving nitroglycerin and receiving placebo, regarding mortality (0 vs. 0%, NS), myocardial infarction (0 vs. 2%, NS), postprocedural chest pain (10 vs. 8%, NS) or repeated PCI (0 vs. 2%, NS). Similarly, 24-month follow-up also revealed no significant differences between those receiving nitroglycerin and placebo (mortality: 0 vs. 0%, NS; myocardial infarction: 4 vs. 4%, NS; repeated PCI: 10 vs. 8%, NS or CABG: 0 vs. 0%, NS). CONCLUSIONS: Routine use of intravenous nitroglycerin after elective PCI has no influence on in-hospital and long-term outcome, including cardiac death, myocardial infarction, postprocedural chest pain, unstable angina and repeated PCI.     

Subcutaneous administration of nitroglycerin to facilitate radial artery cannulation.

OBJECTIVES: To study the effect of sublingual versus subcutaneous nitroglycerin on radial artery spasm caused by failed access attempts. BACKGROUND: Radial artery spasm is the leading reason for failed radial access. We studied the efficacy of systemic versus local nitroglycerin in relieving radial artery spasm caused by needle entry resulting in failed cannulation. METHODS: Fifty-two consecutive patients were studied. All patients had failed attempt at radial artery cannulation, resulting in loss of radial pulse. Patients were divided in three groups, group I (n = 11), observed without additional treatment, group II (n = 20), administered 400 mcg of sublingual nitroglycerin, and group III (n = 21), administered 400 mcg of subcutaneous nitroglycerin at the site of the lost radial pulse. All patients were monitored for the return of radial pulse. Demographics, hemodynamics, and time to return of radial pulse as well as ability to successfully cannulate the radial artery were recorded. RESULTS: Seventy-two percent of group I patients, 90% of group II patients, and 100% of group III patients had re-establishment of radial pulse. The time to return of radial pulse was significantly shorter for group III compared with that for group II (3 +/- 1 min vs. 8 +/- 1 min respectively, P < 0.001). Re-establishment of radial pulse was faster in group II and group III compared with that in group I (18 +/- 5 min, P < 0.001). Systolic blood pressure changes and headaches were less common in group III. CONCLUSION: Subcutaneous administration of nitroglycerin is superior in facilitating radial artery cannulation after initial failed attempt.     

倾斜试验中舌下含服硝酸甘油与静滴异丙肾上腺素的对比研究

102例受试者，包括不明原因晕厥患者72例，无晕厥史的正常人30例，随机分为异丙肾上腺素（ISO）组和硝酸甘油（NG）组，观察倾斜试验中是否可诱发与临床症状相一致的晕厥或晕厥先兆以及相伴随的心率、血压变化。ISO组病人42例，正常人14例，副作用多，常见为心悸（20例，占35．7％），其中4例出现频发室性早搏，不能耐受而终止检查。NG组病人30例，正常人16例，无心悸、心律失常等副作用，仅1例（2．2％）发生头痛，尚可耐受。ISO组敏感性和特异性分别为76.3％、76．9％；NG组为713％、87．5％，两组之间无显著性差异（P＞0．05）。对NG组中的30例随机进行了重复试验，两次均阳性13例，均阴性15例，两次试验的符合率为93.3％（28／30）。表明倾斜试验中舌下含服NG对诊断血管迷走性是厥安全、可靠，有一定临床价值。     

Combined use of nitroglycerin and N-acetylcysteine in the management of unstable angina pectoris

The vasodilator effects of nitroglycerin (NTG) are mediated via activation of guanylate cyclase; this process is believed to require the availability of free sulfhydryl groups. Previous studies in man have shown that the sulfhydryl donor N-acetylcysteine (NAC) potentiates the systemic and coronary vasodilator effects of NTG. Furthermore, interaction of NTG and NAC may lead to the formation of S-nitroso-NAC, which strongly inhibits platelet aggregation. The effects of intravenous NTG combined with intravenous NAC (5 g 6 hourly) were compared with those of intravenous NTG alone in a double-blind trial in 46 patients with severe unstable angina pectoris unresponsive to conventional treatment, which included calcium antagonists and cutaneous nitrates in all but one patient. Treatment with NTG/NAC (24 patients) and that with NTG alone (22 patients) was associated with a similar frequency of episodes of chest pain and of increments in NTG infusion rate for pain control (10 vs 17; p = NS). The NTG/NAC group had a significantly lower incidence of acute myocardial infarction than the NTG/placebo group (three vs 10 patients; p = .013). Symptomatic hypotension occurred frequently in the NTG/NAC group (seven vs 0 patients; p = .006). Lactate-pyruvate ratios and venous NTG concentrations were not significantly affected by NAC. Subsequently, another 20 consecutive patients were treated with intravenous NTG and continuously infused NAC (10 g/day). Seven remained pain free during the first 24 hr of NTG infusion; 11 required increments in NTG infusion rate for pain control. Acute myocardial infarction occurred in one patient, while none developed symptomatic hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nalbuphine versus diamorphine early in the course of suspected myocardial infarction

One hundred and seventy-six consecutive patients with moderate or severe pain of suspected myocardial infarction were randomized to receive nalbuphine less than or equal to 20 mg or diamorphine less than or equal to 5 mg intravenously with metoclopramide 10 mg and were observed over 2 hours. One hundred and forty-two patients (81%) received the test drug outside hospital. The median time from symptom onset to treatment was 135 minutes for the nalbuphine group and 125 minutes for the diamorphine group. Satisfactory pain relief (grade 0 or 1) was similar for both groups at each time assessment. In particular, within 10 minutes of the drug's administration 77% of those receiving nalbuphine and 68% who received diamorphine had satisfactory pain relief. The number of doses of each drug, the number of patients withdrawn from the trial because of unsatisfactory pain relief or recurrence of chest pain were similar for both groups. For those with myocardial infarction there was similar satisfactory pain relief with nalbuphine as diamorphine. No significant deleterious haemodynamic effects or other side-effects occurred. The noncontrolled classification and low addiction potential of nalbuphine allow for its more widespread use in the control of pain of suspected myocardial infarction.     

Incomplete and delayed bioavailability of sublingual nitroglycerin

Eight healthy male volunteers received 16 doses of sublingual nitroglycerin tablets (0.4 mg). After 8 minutes, each subject rinsed out his mouth to halt the drug absorption process. The mouth rinses were assayed by high-performance liquid chromatography for residual nitroglycerin content. Each subject also received intravenous infusions of nitroglycerin so that the absolute bioavailability could be evaluated. Plasma nitroglycerin concentrations were determined using a specific and sensitive capillary gas chromatographic method capable of quantifying 25 pg/ml of nitroglycerin. The mean bioavailability (+/- standard deviation) of sublingual nitroglycerin, estimated from plasma concentrations, was 36.2 +/- 24.9% (range 2.6 to 113%). The amount of drug not absorbed after 8 minutes, as determined from the analysis of the mouth rinses, varied from 2.7 to 65.8% (mean 31.4 +/- 18.9%) of the administered sublingual dose. Mean nitroglycerin peak concentrations of 1.89 +/- 1.64 ng/ml were obtained at a mean peak time of 5.3 +/- 2.3 minutes. Thus, sublingual absorption is not instantaneous and can be relatively slow, with peak times of as long as 10 minutes. These data indicate that nitroglycerin pharmacokinetic values should not be estimated only from sublingual doses. Additionally, attempts to correlate pharmacodynamic measurements to sublingual doses must take into account the low and variable bioavailability and the potentially long peak times after sublingual nitroglycerin administration to patients.     

Vasodilatory effect of subsequent administration of fasudil, a rho-kinase inhibitor, surpasses that of nitroglycerin at the concentric coronary stenosis in patients with stable angina pectoris.

BACKGROUND: Recent studies have suggested that the Rho/Rho-kinase mediated pathway (Rho-kinase pathway) regulates the vasomotion of arteries in pathological conditions. However, it remains unclear regarding whether this pathway regulates the coronary vasomotion of atherosclerotic lesions. METHODS AND RESULTS: The coronary diameter at the concentric stenotic site, which is considered to reflect the whole circumferential atherosclerosis, in patients with stable angina pectoris (SAP; n=11) and the control site in patients with SAP and chest pain syndrome (CPS; n=9), was measured at baseline and after the intracoronary administration of nitroglycerin (200 microg) and the subsequent intravenous infusion of fasudil (30 mg for 30 min), a Rho-kinase inhibitor, during coronary angiography. The change in the diameter with fasudil at the concentric stenotic site (22.0+/-10.0%) was significantly higher than that with nitroglycerin (4.7+/-6.0%, p<0.001) in patients with SAP. Meanwhile, the vasodilatory effect of nitroglycerin and fasudil at the control site was similar in both group of patients (25.5+/-17.3% and 21.9+/-14.9% in SAP and 34.4+/-20.8% and 33.2+/-23.6% in CPS, respectively). CONCLUSIONS: The vasodilatory effect of the subsequent administration of fasudil surpassed that of nitroglycerin at the concentric coronary stenosis in patients with SAP, thus suggesting that the Rho-kinase pathway regulates the coronary vasomotion of atherosclerotic lesions.     

持续静脉泵入呋塞米与多巴胺联合黄芪注射液治疗难治性心力衰竭患者利尿剂抵抗

目的观察持续静脉泵人呋塞米与多巴胺并静脉滴注黄芪注射液对难治性心衰患者利尿剂抵抗的疗效、可行性及安全性。方法将47例产生利尿剂抵抗的难治性心衰患者随机分为对照组20例及治疗组27例。对照组采用常规利尿剂及其他抗心衰治疗;治疗组在常规治疗基础上持续静脉泵入呋塞米和多巴胺及静脉滴注黄芪注射液,连用3-5d。观察治疗前、后两组临床症状体征及胸片肺水肿、肺淤血改善情况,以及心功能指标等方面的变化。结果两组治疗后各项观察指标较治疗前都有改善,但治疗组改善更加明显（P〈O．05）,治疗组临床总有效率为85．2％,对照组为45％（P〈0．05）。结论在常规抗心力衰竭治疗基础上,持续静脉泵人呋塞米与多巴胺辅以黄芪注射液静脉滴注对难治性心衰患者利尿剂抵抗疗效显著,临床安全可行。     

Effects of continuous infusion of intravenous nitroglycerin on methemoglobin levels

The effect of continuous infusion of intravenous nitroglycerin (NTG) on methemoglobin levels in 24 coronary care unit patients was studied. Fifteen patients were admitted with acute myocardial infarction, 5 patients with angina pectoris, 1 patient with congestive heart failure, 2 with chest pain of unknown origin and 1 with chest pain of musculoskeletal origin. Intravenous NTG therapy was initiated at a 5 micrograms/min dose and titrated at 5-micrograms increases until relief of symptoms or until the maximal dose tolerated by each patient. Successive methemoglobin levels were measured at baseline, at each 20 micrograms/min dose increase, at the maximal dose and immediately before weaning the patient from the maximal dose. Statistical analysis by the Student t test (paired samples, p less than 0.05) showed no significant difference between the mean methemoglobin levels at baseline and the mean methemoglobin levels drawn at 20, 40 and 60 micrograms, and before weaning from the maximal dose. No serious adverse effects associated with methemoglobinemia were encountered. It is concluded that intravenous NTG administration in a dose of 0.2 to 2.12 micrograms/min/kg body weight produces no significant methemoglobinemia.     

Role of adenosine in pathogenesis of anginal pain

The intravenous infusion of adenosine provokes anginalike chest pain. To establish its origin, an intracoronary infusion of increasing adenosine concentrations was given in 22 patients with stable angina pectoris. During adenosine infusion, 20 patients had chest pain without electrocardiographic signs of ischemia. They all reported that the chest pain was similar to their usual anginal pain. In 10 of the 22 patients adenosine was also infused into the right atrium, but it never produced symptoms at the doses that had provoked chest pain during intracoronary infusion. In seven other patients, the intracoronary adenosine infusion was repeated after intravenous administration of aminophylline, an antagonist of adenosine P1-receptors. Aminophylline decreased the severity of adenosine-induced chest pain (assessed with a visual analog scale) from 42 +/- 22 to 23 +/- 17 mm (p less than 0.002). In the remaining five of the 22 patients, monitoring of blood oxygen saturation in the coronary sinus during intracoronary adenosine administration showed that maximum coronary vasodilation was achieved at doses lower than those responsible for chest pain. A single-blind, placebo-controlled, randomized trial of the effect of aminophylline on exercise-induced chest pain was also performed in 20 other patients with stable angina. Aminophylline, compared with placebo, decreased the severity of chest pain at peak exercise from 67 +/- 21 to 51 +/- 23 mm (p less than 0.02), despite the achievement of a similar degree of ST-segment depression. Finally, the effect of intravenous adenosine was compared in 10 patients with predominantly painful myocardial ischemia and in 10 patients with predominantly silent ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

静脉滴注地尔硫治疗难治性心绞痛的临床观察

目的　观察静脉滴注地尔硫治疗难治性心绞痛的临床疗效及安全性。方法　10例难治性心绞痛患者停用静脉点滴硝酸甘油及口服β-受体阻滞剂后,静点地尔硫40～150μg/min（2.4～9mg/h）持续48h。结果　与用药前48小时相比,7例患者心绞痛发作显著改善,其中5例完全控制,2例明显改善。3例（30％）无效,经联合应用静脉硝酸甘油后1例完全控制,2例明显改善。无严重低血压、缓慢心律失常及心功能恶化等不良反应发生;无急性心肌梗死、需要急诊介入治疗及死亡发生。8例患者在病情稳定后1周内行介入检查与治疗,其中5例接受PTCA及支架置入术,3例接受冠状动脉旁路移植术。结论　静脉滴注地尔硫40～150μg/min(2.4～9mg/h)或者联合应用静脉硝酸甘油为难治性心绞痛提供了一种较为安全有效的药物治疗手段,值得临床进一步深入探讨。