Silent ischemia predicts infarction and death during 2 year follow-up of unstable angina

Silent myocardial ischemia as detected on Holter electrocardiographic (ECG) monitoring is present in greater than 50% of patients with unstable angina despite intensive medical therapy. The presence and the extent of silent ischemia have been correlated with an increased risk of early (1 month) unfavorable outcome including myocardial infarction and need for coronary revascularization for persistent symptoms. Seventy patients with unstable angina who had undergone continuous ECG monitoring for silent ischemia were followed up for 2 years; 37 patients (Group I) had Holter ECG evidence of silent ischemia at bed rest in the coronary care unit during medical treatment with nitrates, beta-receptor blockers and calcium channel antagonists; the other 33 patients (Group II) had no ischemic ST segment changes (symptomatic or silent) on Holter monitoring. Over a 2 year follow-up period, myocardial infarction occurred in 10 patients in Group I (in 2 it was fatal) compared with one nonfatal infarction in Group II (p less than 0.01 by Kaplan-Meier analysis); revascularization with either coronary bypass surgery or angioplasty for symptomatic ischemia was performed in 11 Group I and 5 Group II patients (p less than 0.05). Multivariate Cox's hazard analysis demonstrated that the presence of silent ischemia was the best predictor of 2 year outcome. Therefore, persistent silent myocardial ischemia despite medical therapy in patients with unstable angina carries adverse prognostic implications that persist over a 2 year period.     

Treatment of stable angina.

Severe atherosclerotic narrowing of one or more coronary arteries is responsible for myocardial ischemia and angina pectoris in most patients with stable angina pectoris. The coronary arteries of patients with stable angina also contain many nonobstructive plaques, which are prone to fissures or rupture resulting in presentation of acute coronary syndromes (unstable angina, myocardial infarction, sudden ischemic death). In addition to symptomatic relief of symptoms and an increase in angina-free walking time with antianginal drugs or revascularization procedures, the recent emphasis of treatment has been to reduce adverse clinical outcomes (coronary death and myocardial infarction). The role of smoking cessation, aspirin, treatment of elevated lipids, and treatment of high blood pressure in all patients and of beta-blockers and angiotensin-converting enzyme inhibitors in patients with diminished systolic left ventricular systolic function in reducing adverse outcomes has been well established. What is unknown, however, is whether any anti-anginal drugs (beta-blockers, long-acting nitrates, calcium channel blockers) effect adverse outcomes in patients with stable angina pectoris. Recent trials evaluated the usefulness of suppression of ambulatory ischemia in patients with stable angina pectoris, but it remains to be established whether suppression of ambulatory myocardial ischemia with antianginal agents or revascularization therapy is superior to pharmacologic therapy targeting symptom relief. Patients who have refractory angina despite optimal medical treatment and are not candidates for revascularization procedures may be candidates for newer techniques of transmyocardial revascularization, enhanced external counterpulsation, spinal cord stimulation, or sympathectomy. The usefulness of these techniques, however, needs to be confirmed in large randomized clinical trials.     

112例不稳定型心绞痛患者介入治疗的临床评价

目的 探讨不稳定型心绞痛患者介入治疗的安全性及临床效果。方法 不稳定型心绞痛112例．反复发作时即行冠状动脉造影,明确病变后对“罪犯”血管行经皮冠状动脉介入治疗,术后残余狭窄小于10％,前向血流按心肌梗死溶栓治疗临床实验（thrombolysisinmyocardialinfarction,TIMI）血流分级3级为手术成功;随访6月,分析即时及远期效果。结果 手术成功率100％,所有病例均随访6月,其中,17例（15％）患者在经皮冠状动脉介入术后3-6个月再发心绞痛,发作时心电图或平板负荷试验提示心肌缺血,此17例均再次冠状动脉造影提示“罪犯”血管支架内再狭窄,再次行经皮冠状动脉介入术。其余病例术后6个月内未再发心绞痛。随访期间无1例再发心肌梗死或死亡。结论 早期介入治疗不稳定型心绞痛患者是有效的治疗方法,手术成功率及安全性高,近期和远期临床效果满意。     

Visceral chest pain in unstable angina pectoris and effects of transcutaneous electrical nerve stimulation (TENS)

A substantial proportion of patients with chest pain referred to hospital, show signs of coronary artery disease. Anginal pain could be conceptualized as a warning signal for coronary artery disease and impending death. But, for many reasons this theory is partly disputed. Firstly, not all ischemic episodes are accompanied by anginal pain (silent ischemia). Secondly, chest pain indistinguishable from true angina pectoris may be the result of other abnormalities of thoracic viscera. Nevertheless acute severe cardiac ischemia often gives rise to anginal chest pain. Unstable angina pectoris is carrying a higher risk for future events in spite of intensive medical treatment. A special problem are patients awaiting coronary intervention because of severe ischemia and maximum medical treatment, who experience ischemic pain. New treatment regimens are needed for these patients. This review discusses the symptom of visceral pain from the heart, angina pectoris, its relation to ischemia and unstable angina pectoris. It also addresses the role of afferent nerve stimulation (transcutaneous electrical nerve stimulation, TENS) in the treatment of severe angina pectoris as well as recent findings of TENS applicability in unstable angina.     

Calcium antagonists for Prinzmetal's variant angina, unstable angina and silent myocardial ischemia: therapeutic tool and probe for identification of pathophysiologic mechanisms

The calcium antagonists provide a unique tool to reduce myocardial oxygen demand and prevent increases in coronary vasomotor tone. For patients with Prinzmetal's variant angina, diltiazem, nifedipine and verapamil are extremely effective in preventing episodes of coronary vasospasm and symptoms of ischemia. Unstable angina pectoris is a more complex pathophysiologic syndrome with episodes of ischemia due to increases in coronary vasomotor tone, intermittent platelet aggregation or alterations in the underlying atherosclerotic plaque. Each of the calcium antagonists is effective as monotherapy in decreasing the frequency of angina at rest. Nifedipine is the only calcium antagonist that has been studied in a combination regimen with beta blockers and nitrates for patients with unstable angina, and control of angina is better with the combination regimen than with either form of therapy alone. Although symptoms of myocardial ischemia in unstable angina are reduced by calcium antagonists, these agents do not seem to decrease the incidence of adverse outcomes. Antiplatelet therapy appears to improve morbidity and mortality in patients with unstable angina, suggesting that thrombus formation may play a central role in that disorder. Episodes of silent or asymptomatic myocardial ischemia, identified by ST-segment monitoring, occur in a variety of disorders of coronary disease. Among patients with Prinzmetal's variant angina and unstable angina, episodes of silent ischemia appear to be as frequent as episodes of angina and the calcium antagonists are effective in decreasing episodes of ischemia regardless of the presence or absence of symptoms. Persisting episodes of silent ischemia among patients with unstable angina despite maximal medical therapy identify patients at high risk for an early unfavorable outcome. Among patients with stable exertional angina, episodes of silent ischemia may be up to 5 times as frequent as episodes of angina, and may be due to increases in coronary vasomotor tone, transient platelet aggregation or increases in myocardial oxygen demand. Preliminary experience suggests that calcium antagonists and beta blockers are effective in decreasing episodes of silent ischemia in patients with stable exertional angina and that a combination regimen may be more effective than either form of therapy alone.     

Ventricular arrhythmias during unstable angina pectoris.

In order to study the occurrence and frequency of ischemia-induced ventricular arrhythmias, we analyzed 105 episodes of spontaneous angina pectoris occurring at rest in 28 hospitalized patients with unstable angina pectoris and proved coronary artery disease. Of 24 patients with serious ventricular arrhythmias during pain, 17 (57%) were arrhythmia-free during monitoring. In the other four patients, 17 of 29 (59%) pain episodes were associated with serious ventricular arrhythmias, and three of these four had serious ventricular arrhythmias during pain-free periods. Each patient tended to manifest the same type of arrhythmia during repeat episodes of pain. It appears that continuous electrocardiogram (ECG) monitoring is important during the initial hospitalization of the patient with unstable angina. The presence of ventricular arrhythmias during pain-free periods indicates a high risk for serious ventricular arrhythmias during episodes of spontaneous pain. These patients should be considered for continued ECG monitoring and antiarrhythmic therapy.     

Exercise echocardiography after stabilization of unstable angina: correlation with exercise thallium-201 single photon emission computed tomography.

The diagnostic usefulness of predischarge exercise echocardiography in 35 patients with unstable angina who responded to medical therapy was correlated with exercise thallium-201 single photon emission computed tomography (TI-SPECT) performed, on the average, three days after the exercise echocardiography. None of the patients had myocardial infarction prior to hospitalization or before TI-SPECT and none had left bundle-branch block on their rest electrocardiogram (ECG). Exercise echocardiography was positive in 21 patients and TI-SPECT in 24. The results of the two techniques were concordant in 28 of 35 patients (agreement = 80%, k = 0.57 +/- 0.14, p less than 0.001). Wall-by-wall comparison of the distribution of exercise-induced wall motion abnormalities with reversible thallium defects showed complete or partial correlation in all of 19 patients in whom both the tests were positive. A positive exercise ECG and positive exercise echocardiography identified 11 of 11 patients with angiographically verified significant coronary artery disease (CAD) and 11 of 12 patients (92%) with positive TI-SPECT. Thus, exercise echocardiography is a valuable addition to routine predischarge exercise test in the noninvasive diagnosis of myocardial ischemia and shows a good correlation with TI-SPECT in detecting and localizing ischemia in patients with unstable angina stabilized on medical therapy.     

低分子肝素治疗不稳定型心绞痛疗效观察

目的:观察低分子肝素治疗不稳定型心绞痛疗效。方法:选择诊断明确的不稳型心绞痛患者62例,随机分为治疗组(32例)和对照组(30例),对照组采用硝酸酯制剂、β受体阻滞剂、钙道阻滞剂、肠溶阿司匹林等常规药物治疗,治疗组在以上治疗的基础上加用低分子肝素,观察两组对心绞痛的疗效。结果:治疗组临床症状明显改善,心电图缺血性ST段下移明显改善,且优于对照组,P均<0．05。结论:低分子肝素治疗不稳定型心绞痛疗效肯定,安全,优于常规抗心绞痛治疗。     

Unstable angina: the case for operation.

From July 1975 through September 1977, surgical revascularization was performed in 95 consecutive patients with unstable angina, 53 at high risk (defined as in-hospital pain at rest with reversible ischemic electrocardiographic changes) and 42 at low risk (defined as pain at rest remitting upon hospitalization). Historical, electrocardiographic and cardiac catheterization data were similar in both groups; however, patients at high risk required large doses of propranolol, and one patient needed additional intraaortic counterpulsation for preoperative stabilization of ischemia. Proximal left anterior descending (79 patients) and left main (15 patients) coronary artery disease with abnormal ventricular function characterized both groups of patients with unstable angina. Revascularization (2.5 grafts/patient) was performed with hypothermia and intermittent ischemic arrest. Complications included one death and three perioperative infarctions. No patient needed inotropic support. No late deaths occurred in a follow-up period of up to 30 months. The data indicate that (1) “prophylactic” preoperative intraaortic balloon counterpulsation in patients with unstable angina, although advocated by some surgeons, is unnecessary; (2) the very small incidence of complications when unstable angina—particularly high risk unstable angina—is managed as outlined strongly suggests that surgical revascularization is definitive therapy; and (3) the therapeutic implications of large scale controlled studies of medical versus surgical therapy for unstable angina, which include results achieved 3 or 4 years ago and describe significantly higher rates of mortality and infarction than those reported here and by others, may not be pertinent to therapeutic decisions made today.     

Unstable angina pectoris: National cooperative study group to compare medical and surgical therapy: I. Report of protocol and patient population

A preliminary report is presented of a prospective randomized trial conducted by eight cooperative institutions under the auspices of the National Heart and Lung Institute to compare the effectiveness of medical and surgical therapy in the management of the acute stages of unstable angina pectoris. To date 150 patients have been included in the randomized trial, 80 assigned to medical and 70 to surgical therapy; the clinical presentation, coronary arterial anatomy and left ventricular function in the two groups are similar.Some physicians have been reluctant to prescribe medical or surgical therapy by a random process, and the ethical basis of the trial has been questioned. Since there are no hard data regarding the natural history and outcome of therapy for unstable angina pectoris, randomization appears to provide a rational way of selecting therapy. Furthermore, subsets of patients at high risk may emerge during the process of randomization. The design of this randomized trial is compared with that of another reported trial.Thus far, the study has shown that it is possible to conduct a randomized trial in patients with unstable angina pectoris, and that the medical and surgical groups have been similar in relation to the variables examined. The group as a whole presented with severe angina pectoris, either as a crescendo pattern or as new onset of angina at rest, and 84 percent had recurrence of pain while in the coronary care unit and receiving vigorous medical therapy. It is anticipated that sufficient patients will have been entered into the trial within the next 12 months to determine whether medical or surgical therapy is superior in the acute stages of unstable angina pectoris.     

Increased levels of monocyte-related cytokines in patients with unstable angina

Inflammatory cytokines play important roles in coronary artery disease. We investigated the clinical significance of monocyte-related cytokine expression in patients with angina pectoris. We studied 26 patients with stable effort angina and 20 patients with unstable angina in whom stenotic lesions of the coronary arteries were confirmed by selective coronary angiography. Plasma levels of interleukin-6 (IL-6), macrophage colony stimulating factor (MCSF), and monocyte chemoattractant protein-1 (MCP-1) were measured. Plasma levels of IL-6, MCSF, and MCP-1 in patients with unstable angina were significantly higher than those in patients with stable angina or control subjects. Patients with unstable angina were further divided into sub-groups according to their clinical classification; Levels of IL-6, MCSF, and MCP-1 in patients, who had anginal attacks at rest within the 48 h prior to admission (Braunwald class IIIB) were significantly higher than those in patients, who did not have attacks at rest (class IB). Five unstable patients, who were refractory to medical therapy and were referred for emergency coronary revascularization showed marked elevation of plasma MCSF and MCP-1 levels. In conclusion, plasma levels of monocyte-related cytokines were elevated in unstable angina. These increases were marked in patients with unstable angina with recent ischemic attack at rest, suggesting that activation of monocytes is involved in vulnerability of underlying atheromatous plaque.     

Treatment of refractory angina pectoris

Refractory angina pectoris is defined as Canadian Cardiovascular Society class III or IV angina, where there is marked limitation of ordinary physical activity or inability to perform ordinary physical activity without discomfort, with an objective evidence of myocardial ischemia and persistence of symptoms despite optimal medical therapy, life style modification treatments, and revascularization therapies. The patients with refractory angina pectoris may have diffuse coronary artery disease, multiple distal coronary stenoses, and or small coronary arteries. In addition, a substantial portion of these patients cannot achieve complete revascularization and continue to experience residual anginal symptoms that may impair quality of their life and increase morbidity. This represents an end-stage coronary artery disease characterized by a severe myocardial insufficiency usually with impaired left ventricular function. As the life expectancy is increasing, patients with angina pectoris refractory to conventional antianginal therapeutics are a challenging problem. We review the nonconventional therapies to treat the refractory angina pectoris, including pharmacotherapy, therapeutic angiogenesis, transcutaneus electrical nerve and spinal cord stimulation, enhanced external counterpulsation, surgical transmyocardial laser revascularization, percutaneous transmyocardial laser revascularization, percutaneous in situ coronary venous arterializations, and percutaneous in situ coronary artery bypass. These therapies are not supported by a large body of data and have only a complementary role; therefore, the aggressive traditional and proven treatment of angina pectoris should be continued along with these therapies, used on an individual basis.     

Pseudostabilization of unstable angina pectoris: disappearance of symptoms in persistence of silent myocardial ischemia

We studied a patient hospitalized with unstable angina pectoris; ST-segment analysis during Holter ECG revealed several silent ischemic attacks despite complete disappearance of anginal symptoms under medical treatment. Prior to cardiac catheterization the patient went into acute myocardial infarction. Immediate intravenous thrombolysis and subsequent angioplasty of a high-grade stenosis abolished the ischemic events. ST-segment analysis during Holter ECG offers a method to detect ischemic events despite the disappearance of anginal symptoms in the clinical course of unstable angina pectoris. This technique might therefore identify patients with unstable angina pectoris at higher risk for further cardiac events.     

Akute Koronarsyndrome – ein Update Teil II: Koronare Revaskularisation und Risikostratifizierung

CORONARY REVASCULARIZATION: PTCA in patients with refractory unstable angina is associated with a substantial risk of the following complications: death, myocardial infarction, need for emergency surgery, and restenosis. The introduction of intracoronary stents, however, has improved both short-term and long-term outcomes. The newer adjunctive pharmacologic therapies enhance even further the benefits associated with the use of stents. The decision regarding the specific revascularization procedure to be used (e.g., CABG, PTCA, stent placement, or atherectomy) is based on the coronary anatomy, the left ventricular function, the experience of the medical and surgical personnel, the presence or absence of coexisting illnesses, and the preferences of both the patient and the physician. RISK STRATIFICATION: Among patients with unstable angina or non-Q-wave myocardial infarction, there is an increased risk of death within 6 weeks in those with elevated troponin I levels and the risk of death continues to increase as the troponin level increases. Reversible ST segment depression is associated with an increase by a factor of 3-6 in the likelihood of death, myocardial infarction, ischemia at rest, or provocable ischemia during a test to stratify risk. Exercise or pharmacologic stress testing provides important information about a patient's risk. Although the conditions of the majority of patients with unstable angina will stabilize with effective antiischemic medications, approximately 50-60% of such patients will require coronary angiography and revascularization because of the "failure" of medical therapy. High-risk patients are those who have had angina at rest, prolonged angina, or persistent angina with dynamic ST segment changes or hemodynamic instability, and they urgently require simultaneous invasive evaluation and treatment. Medical therapy should be adjusted rapidly to relieve manifestations of ischemia and should include antiplatelet therapy (aspirin, or ticlopidine or clopidogrel if aspirin is contraindicated), antithrombotic therapy (unfractionated heparin or low-molecular-weight heparin), beta-blockers, nitrates, and possibly calcium-channel blockers. Early administration of glycoprotein IIb/IIIa inhibitors may be particularly important, especially in high-risk patients with positive troponin tests or those in whom implantation of coronary stents is anticipated.     

Clinical significance of silent ischemia in unstable angina pectoris

In a prospective study the significance of silent ischemia was evaluated in 66 patients with a clinical diagnosis of unstable angina (no requirement for reversible ST-T changes during pain on 12-lead electrocardiograms before entry), and the results of continuous 2-channel electrocardiographic (ECG) recordings, begun within 24 hours of admission, were compared with other clinical and ECG predictors of adverse outcome. Ischemic changes were detected in 7 patients (11%) during a mean of 41 hours of recording. There were 37 episodes of transient ST-segment change (16 ST elevation, 21 ST depression) of which 11 (30%) were symptomatic and 26 (70%) were silent. All 7 patients had at least 1 silent episode and 5 also had symptomatic episodes during the recording but only 2 patients had exclusively silent episodes. During a mean follow-up of 13.3 months, 3 patients died, 5 had a nonfatal myocardial infarction and 32 required revascularization. Although transient myocardial ischemia during the continuous ECG recording, whether silent or symptomatic, was a specific predictor of subsequent nonfatal myocardial infarction or death (specificity 92%), its sensitivity for these events was low (25%). In contrast, recurrent rest pain (greater than or equal to 1 episode) occurred in all patients with these serious adverse events (sensitivity 100%, specificity 49%). Transient ischemia occurs infrequently during continuous ECG recordings in patients with unstable angina not selected by reversible ST-T changes on a 12-lead electrocardiogram at entry. Recurrent rest pain after hospital admission is a more sensitive predictor of serious events in this group.     

Asymptomatic myocardial ischemia

Silent (asymptomatic) myocardial ischemia (SMI) is defined as a transient alteration in myocardial perfusion in the absence of chest pain or the usual anginal equivalents. Patients may be classified as having one of the three types of SMI: type A--totally asymptomatic patients with no history of angina or myocardial infarction; type B--asymptomatic patients with previous myocardial infarction; type C--patients with angina and asymptomatic ischemic episodes. SMI has been found in 2.5% of all healthy males aged 40-59 and in 20% of all postinfarction patients. In type C-patients, 80% has been found to have asymptomatic ischemic episodes in addition to typical angina pectoris. The frequency of SMI may be up to three or four times that of anginal attacks. SMI patients have generally reduced sensitivity to pain an differences in severity an duration of ischemic episodes. Diagnosis is based on screening by means of exercise testing in patients working in specific professions (like pilots, busdrivers etc.), in postinfarction patients and in patients after unstable angina pectoris and after coronary bypass surgery or coronary angioplasty. Prognosis is the same as in asymptomatic ischemia. SMI is an indicator of instability in certain groups of patients (post infarction, after unstable angina pectoris). SMI persisting after medical therapy of unstable angina is associated with adverse short-term-prognosis, therefore coronary surgery or angioplasty is indicated.     

Nitrates for unstable angina

Summary The termunstable angina encompasses heterogeneous clinical syndromes. Fissuring of an atherosclerotic coronary artery plaque with superimposed platelet deposition, with or without additional thrombus formation, is invariably responsible for a prolonged episode of angina at rest, increasing frequency of angina at rest, or with minimal exertion of less than 4 weeks in duration and early postinfarction angina. Plaque progression, rather than plaque fissuring, is the most likely mechanism for progressive reduction in walking distance due to angina in patients who previously have stable angina. Coronary artery spasm is responsible for Prinzmetal's variant angina, but its exact role in other forms of unstable angina is unknown. The mainstay of treatment of unstable angina (prolonged episode of angina at rest and recent onset angina at rest, or with minimal exertion with a crescendo pattern) is aspirin, heparin, or both. Both aspirin and intravenous (IV) heparin or their combination reduce early mortality and the incidence of acute myocardial infarction in patients hospitalized with unstable angina. However, these agents do not promptly relieve chest pain. There are no placebo-controlled studies evaluating the usefulness of nitrates in unstable angina. In open-label studies, continuous therapy with IV nitroglycerin (NTG) for 24 hours or longer has been shown to relieve chest pain in patients with rest angina refractory to therapy with other antianginal agents, including long-acting nitrates. Recurrence of chest pain in patients receiving IV NTG is a common problem and probably represents development of pharmacologic tolerance, but this can be overriden by dose escalation; protracted tolerance during short-term use of IV NTG is usually not a problem. In the acute phase of unstable angina, IV NTG is the preparation of choice as the dose can be rapidly titrated up or down. There is no role of intermittent nitrate therapy in the acute phase of unstable angina. Once the patient is stable for 12–24 hours, IV NTG should be tapered gradually and intermittent therapy with a long-acting nitrate, as outlined for the treatment of stable angina, instituted. Aspirin reduces mortality and morbidity during long-term therapy and should be continued indefinitely. Routine use of morphine and other potent analgesics is not recommended. Patients who do not respond to IV NTG or in whom IV NTG is contraindicated should be treated with a beta-blocker devoid of intrinsic sympathomimetic activity, provided there are no contraindications to beta-blocker therapy. The role of calcium channel blockers in patients nonresponsive to IV NTG is less well defined. In patients already receiving beta-blockers and nitrates, the addition of nifedipine may be beneficial. However, monotherapy with nifedipine or other first-generation dihydropyridines is not recommended. Although there are no large trials of diltiazem or verapamil in unstable angina, these agents are often used in patients who are not candidates for beta-blocker therapy. Patients who are refractory to intensive medical therapy are candidates for coronary angiography and revascularization procedures, provided the coronary anatomy is suitable for such procedures.     

Medical management of significant coronary angiographic stenoses: outcome of 60 patients observed for 433 patient years

BACKGROUND: Percutaneous transluminal coronary angioplasty (PTCA) has become routine in the management of patients with stable angina pectoris and significant coronary stenoses, while medical management of such patients has declined. HYPOTHESIS: The purpose of the present study was to evaluate the outcome of 60 patients at the Virginia Heart Institute with stable angina pectoris, observed between 1976 and 1997, who had documented evidence of severe angiographic disease but were elected to be monitored and managed in an outpatient pharmacologic rehabilitation program. METHODS: Sixty patients with significant stenoses by coronary angiography (21 with single-vessel, 26 with double-vessel, and 13 with triple-vessel) without impaired ventricular function, exercise-induced ischemia or hypotension, limited exercise performance, malignant arrhythmias, or drug intolerance were enrolled in a program of pharmacologic rehabilitation and observed for an average of 7.2 years. RESULTS: Among the 60 patients, there were 6 deaths at a mean interval of 8.3 years. Two deaths were in patients ineligible for revascularization. Another patient who died had refused revascularization after new-onset left ventricular dysfunction, and another died intraoperatively during abdominal aortic aneurysm repair. Two patients died while exercising. Thirteen patients underwent follow-up catheterization for worsening angina; 11 of 13 showed progression, predominantly from new lesions. Four of 11 were referred for revascularization; 7 of 11 continued medical treatment; 49 patients were stable on medical therapy throughout the period of observation. CONCLUSION: Medical management of selected patients with significant coronary stenoses is safe and effective.     

Ventricular arrhythmias in patients with rest angina: correlation with ST segment changes and extent of coronary atherosclerosis

Major ventricular arrhythmias occurring concurrently with myocardial ischemia are presumed to be the most frequent mechanism for sudden cardiac death. Two hundred eighteen catheterized patients with angina pectoris at rest were reviewed to identify clinical, ECG, and arteriographic features that might correlate with the presence of serious ventricular arrhythmias occurring during episodes of rest pain. Ventricular arrhythmias during episodes of rest pain were significantly more common in patients who manifested transient ST segment elevation in the anterior leads and in patients with marked transient ST segment shifts (greater than 5 mm). Ventricular arrhythmias during episodes of rest pain were not more common in patients with extensive coronary artery disease.     

The American Heart Journal: Enhanced service to the cardiovascular community

Seventeen patients presenting with unstable angina pectoris underwent percutaneous transluminal coronary angioplasty (PTCA). Despite vigorous medical therapy, all patients were disabled with 10 experiencing refractory in-hospital angina. PTCA was judged successful in 13 patients and resulted in decreased coronary diameter narrowing from 80 ± 16% to 34 ± 13% and reduced transstenotic pressure gradient from 69 ± 13 to 23 ± 12 mm Hg. Regional coronary blood flow (CBF) and myocardial metabolism were assessed at rest and during pacing tachycardia in six patients with left anterlor descending coronary stenosis. Prior to PTCA, neither regional CBF increased nor coronary vascular resistance declined during rapid pacing; myocardial lactate extraction fell, indicating a shift from aerobic to anerobic metabolism. Following PTCA, however, rapid pacing resulted in increased regional CBF, decreased coronary vascular resistance, and preservation of aerobic metabolism. Following PTCA, successfully dilated patients demonstrated marked relief of angina symptoms, increase in functional capacity, and objective exercise ECG and thallium scintigraphic evidence of relief of previously ischemic myocardium. This investigation demonstrates that PTCA, when combined with medical therapy, can be performed safely and successfully in selected patients who present with otherwise refractory unstable angina, and indicates the procedure deserves further study as a therapeutic alternative in this condition.