Chest pain after coronary artery stent implantation

A sizeable proportion of patients who undergo successful coronary artery stent implantation experiences chest pain immediately after the procedure and/or in the following months in the absence of in-stent restenosis. We investigated this phenomenon in 57 consecutive patients with stable angina who underwent successful stent implantation. Chest pain characteristics were assessed before stent implantation and during 6-month follow-up. All patients underwent coronary angiography within 6 months of the procedure 48 hours after exercise thallium-201 perfusion scintigraphy. Patients who did not exhibit in-stent restenosis underwent an ergonovine test at the end of routine coronary angiography. During follow-up, 15 patients complained of chest pain. Six of these patients exhibited scintigraphic evidence of myocardial ischemia and in-stent restenosis at angiography. In the remaining 9 patients, chest pain occurred in the absence of in-stent restenosis at angiography. In 8 of these patients intracoronary ergonovine administration reproduced their habitual pain, whereas it did not cause any pain in the 42 patients who were completely asymptomatic at follow-up and without in-stent restenosis. Ergonovine caused more intense vasoconstriction and nitroglycerin caused more intense vasodilation of the reference coronary diameter in patients with than in patients without ergonovine-induced pain (-17 +/- 3 vs -9 +/- 3%, p <0.001; 9 +/- 6 vs 5 +/- 4%, p <0.02, respectively). In conclusion, chest pain with features similar to habitual angina occurs in the absence of in-stent restenosis in 1/5 of patients after stent implantation and appears to be associated with more intense coronary vasoreactivity.     

冠状动脉支架术后的胸部不适与再狭窄

目的 :了解冠状动脉支架术后胸部不适与再狭窄关系。方法 :选择接受冠状动脉支架术并在 6个月内进行了冠状动脉造影检查的 186例患者 ,对术后胸部不适和无胸部不适患者进行冠心病易患因素和术后再狭窄比较。结果 :胸部不适和无胸部不适者术后支架内再狭窄的百分率分别为 2 1.4 %和 15 .2 % ,两组的再狭窄率差异无显著性意义。结论 :冠状动脉支架术后的胸部不适除与再狭窄有关外 ,可能与血管内皮功能紊乱及血管的反应性有关。     

Prediction of death after percutaneous coronary interventional procedures

BACKGROUND: The prediction and comparison of procedural death after percutaneous coronary interventional procedures is inherently difficult because of variations in case mix and practice patterns. The impact of modern, expanded patient selection criteria, and newer technologic approaches is unknown. Our objective was to determine whether a risk equation based on patient-related variables and derived from an independent data set can accurately predict procedural death after percutaneous coronary intervention in the current era. METHODS AND RESULTS: An analysis was made of the Mayo Clinic Coronary Interventional Database January 1, 1995, to October 31, 1997. Expected mortality rate was calculated with the use of the New York State multivariate risk score. In 3387 patients, 3830 procedures (55.1% stents) were performed, with an expected mortality rate of 2.32% and observed mortality rate of 2.38% (P = not significant). The risk score derived from the New York multivariate model was highly predictive of death (chi-square = 213.8; P <.0001). The presence of a high-risk lesion characteristic such as calcium, thrombus, or type C lesion was modestly associated with death. CONCLUSIONS: The New York State multivariate model accurately predicted procedural death in our database.     

Peripheral vascular complications after conventional and complex percutaneous coronary interventional procedures.

To determine whether complex cardiovascular interventional procedures (including coronary stent implantation, directional atherectomy, aortic valvuloplasty, and the use of an intraaortic balloon pump or cardiopulmonary bypass support) are associated with an increased likelihood of vascular access site complications, 2,400 consecutive cardiac catheterization procedures were prospectively screened over a 12-month study period. Complications occurred in 35 patients after 39 procedures (1.6%) and included the need for vascular surgical repair (17 patients), blood transfusion (28 patients) and systemic antibiotic therapy (7 patients). The incidence of complications after 1,519 diagnostic studies was 0.6%, after 698 conventional coronary balloon angioplasties 2.6%, and after 183 complex interventions 6.0% (p less than 0.0001); 43% of the complications occurred after procedures of greater than 2 hours' duration and 14% occurred in patients in whom arterial sheaths remained in situ for greater than 24 hours. Detailed demographic and procedural characteristics were compared between the 35 patients with vascular complications and 150 patients randomly drawn from a computerized database of the uncomplicated procedures performed during the screening period. By univariate analysis with correction for multiple comparisons, variables predicting the likelihood of vascular complications included: periprocedural use of heparin (p less than 0.001) or fibrinolytic therapy (p less than 0.001), arterial sheath size greater than or equal to 8Fr (p less than 0.001), patient age greater than or equal to 65 years (p = 0.01), and the presence of peripheral vascular disease (p = 0.03). The results of this study suggest that the overall incidence of access site complications is low but increases with the use of complex cardiovascular interventional procedures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Peripheral vascular complications following coronary interventional procedures

We report the incidence, diagnosis, prevention, and treatment of peripheral vascular complications following coronary interventional procedures as reviewed in the English-language literature. Peripheral vascular complications include hematomas, pseudoaneurysms, arteriovenous fistulae, acute arterial occlusions, cholesterol emboli, and infections that occur with an overall incidence of 1.5–9%. Major predictors of such complications following coronary interventional procedures include advanced age, repeat percutaneous transluminal coronary angioplasty, female gender, and peripheral vascular disease. Minor predictors include level of anticoagulation, use of thrombolytic agents, elevated creatinine levels, low platelet counts, longer periods of anticoagulation, and use of increased sheath size. Ultrasound-guided compression repair of pseudoaneurysms and arteriovenous fistulae are discussed, as are newer methods of treatment such as hemostatic puncture closure devices. Anticipation and early recognition of possible peripheral vascular complications in conjunction with careful attention to the optimal activated clotting time for sheath removal following coronary interventional procedures may translate into fewer vascular complications as well as into shorter and less costly hospital stays.     

Chest pain after nontransmural infarction: the absence of remediable coronary vasospasm

To assess the contribution of coronary vasospasm to chest pain in patients with nontransmural myocardial infarction, we performed a controlled trial of prophylactic antivasospastic therapy. Fifty patients with nontransmural infarction received either nifedipine or placebo in a double-blind randomized trial. Chest pain occurred in 52% of treated patients (38 episodes on 35 days) compared to 48% of control patients (42 episodes on 33 days). Concurrent therapy was comparable in the two groups. Recurrent infarction occurred in 12% and was comparable between groups. Ejection fraction was similar and was unchanged throughout the study in both groups. Logistic regression failed to identify predictors for recurrent chest discomfort. These data indicate that potent antivasospastic therapy does not reduce the incidence of recurrent chest pain or infarction. Thus, remediable coronary vasospasm is not likely to be a major cause of post infarction ischemia in patients with nontransmural infarction.     

Chest pain: coronary or esophageal?

Although it is often relatively easy for the clinician to differentiate between the heart and the esophagus as sources of chest pain, there remains a substantial minority of patients in whom this task is difficult. We have attempted to review points of differential significance which can be elicited through assessment of the patient's symptoms. Diagnostic studies for the detection of esophageal disorders have been reviewed, and the relative usefulness of these studies has been emphasized. As the result of advancements in diagnostic techniques as well as better understanding of esophageal pathophysiology, the clinician is now capable of accurately identifying the esophagus as the source of chest pain.     

重组组织型纤溶酶原激活剂加补救性冠状动脉介入术与直接冠状动脉介入术对急性心肌梗死的疗效研究

目的：为比较急性心肌梗死（AMI）患应用重组组织型纤溶酶原激活剂（rt-PA)50mg治疗，加补救性经皮冠状动脉腔内成形术（PTCA）或冠状动脉内支架（Stent）置入术与直接PTCA／Stent置入术临床疗效。方法：135例首次AMI患随机给予以静脉rt-PA溶栓加补救性PTCA／Stent(A组）和直接PTCA／Stent(B组）。68例患用阿司匹林和肝素后，接受rt-PA50mg治疗，67例直接PTCA和支架。行急诊冠状动脉造影 （CAG），以TIMI血流分级法评估，必要时做PTCA／Stent。本研究终点包括分析两组患的梗死相关血管（IRA）开通率，并发症发生率、病死率及左心室功能。结果：A组IRA开通率为91．0％，B组IRA开通率95．5％。患于首次PTCA前及在3周后用超声心电图测定两组患左心室射血分数（LVEF）。两组患到达导管室时IRA血流已达TIMI3级（n=34其中A组24例，B组10例），最初和恢复期EF值分别为60．8％和62．5％，经介入治疗后变为TIMI3级（n=80），其中A组75％（33／44），B组为84．2％（47／57），最初EF57．0％和恢复期EF57．2％。从未获TIMI3级（n=21），其最初EF54．1％和恢复期EF53．2％为最低。结论：溶栓剂rt-PA50mg治疗加补救性PTCA／Stent与直接PTCA／Stent,在AMI中的疗效比较，可使IRA开通，有利于保护AMI患的左心室功能和不增加副作用。     

Applications of coronary flow velocity during angioplasty and other coronary interventional procedures

Previous studies utilizing Doppler catheters to assess blood flow immediately following coronary artery interventions have failed to demonstrate significant improvement in proximal coronary artery velocities or vasodilator reserve. Measurement of Mood flow velocity, flow reserve, and the phasic diastolic/systolic velocity ratio in the distal coronary artery has been performed following various interventional procedures utilizing a low profile (.018 in) Doppler angioplasty guidewire. Following balloon angioplasty in 38 patients, average peak velocity increased significantly from 19 ± 12 to 35 ± 16 cm/sec in the distal coronary artery. The diastolic/systolic flow ratio improved from 1.3 ± 0.5 to 1.8 ± 0.5 and coronary flow reserve remained unchanged. Similar improvement in distal mean velocities (200%) versus proximal mean velocities (90% increase), and improvement in phasic velocity patterns, total velocity integral, and peak diastolic velocity were also noted in a separate study of 29 patients, before and after balloon angioplasty.Following excimer laser angioplasty in 10 patients, average peak velocity in the distal coronary artery was noted to increase from 6.3 to 13.0 cm/sec following laser alone, with a further increase to 20.6 cm/sec following adjunctive balloon angioplasty. The diastolic/systolic flow ratio increased from a mean value of 1.1 to 2.0 following laser recanalizatkm, with a further increase to 2.9 following adjunctive balloon angioplasty. Following directional coronary atherectomy only modest improvement in distal average peak velocity was noted (24.7 to 33.2 cm/sec), with no significant change in diastolic/systolic velocity ratio (1.78 vs 2.04) immediately following the procedure. Measurement of distal flow velocity parameters performed immediately following coronary interventions may prove useful in assessing the hemodynamic result of these interventions and may prove useful in clinical decision making.     

Chest pain centers: diagnosis of acute coronary syndromes

Chest pain centers in the emergency department have generally been accepted as a safe, cost-effective, and rapid approach to the evaluation, triage, and management of patients with potential acute coronary syndromes. These centers were initially designed to enhance patient care by decreasing time to treatment for acute myocardial infarction (AMI) and rapidly identifying patients with unstable angina. They also included community outreach and educational objectives designed to reduce time from the onset of chest pain to ED presentation. In the past decade, health care financial constraints have created additional impetus to the development of chest pain centers. Cost reduction efforts have occurred to reduce hospitalizations, lengths of stay, and unnecessary treatments and procedures. Practitioners and administrators try to balance these goals with the imperative to provide high-quality patient care. Protocol-driven approaches have been developed for specific disease processes in emergency settings. The chest pain center concept is such an approach for patients with chest pain. Chest pain is the second most common ED presenting complaint and is a symptom related to the leading cause of death in the United States, coronary artery disease (CAD). One third of ED patients with chest pain will eventually have a diagnosis of acute coronary syndrome. Many patients with acute coronary syndromes have atypical presentations that are not diagnosed in the ED with the traditional diagnostic evaluation of a history, physical examination, and 12-lead ECG. If they are not admitted to the hospital for further evaluation, the diagnosis may be missed. The 2% to 5% of AMI patients who are inadvertently released home often have poor outcomes and result in a leading cause of malpractice suits in emergency medicine. More than one half of ED patients with chest pain have clinical findings after their initial evaluation consistent with acute coronary syndromes and are admitted to the hospital. Approximately one half of these patients, after evaluation in the hospital, are found not to have acute coronary syndromes. The cost for these negative inpatient cardiac evaluations has been estimated to be $6 billion in the United States each year. Today, chest pain centers serve as an integral component of many EDs. Their success and safety is the result of a focused, protocol-driven approach directed at the acute coronary syndrome continuum from unstable angina to transmural Q-wave myocardial infarction. New therapies for acute coronary syndromes make ED triage and risk stratification increasingly important. Although different chest pain center protocols have proved effective, all address the diagnosis and rapid treatment of acute myocardial necrosis, rest ischemia, and exercise-induced ischemia. Identifying patients with coronary artery disease in one of these stages in the spectrum of myocardial ischemia is the foundation for a successful chest pain center in the ED.     

Chest pain and behavior in suspected coronary artery disease

This study assessed behavioral activity, dietary and emotional variables among patient cohorts with angina pectoris, atypical chest pain, and no chest pain in whom coronary disease is suspected. Questionnaire responses of 3,899 employed male patients at the time of coronary arteriography were analyzed. Patients with angina pectoris had high levels of coronary-prone and neurotic attitudes, and fatigue variables including feeling unrested on awakening, easy fatiguability, reducing activity at work and arriving home tired. Atypical chest pain patients showed coronary-prone and neurotic attitudes similar to the angina pectoris group but had less coronary occlusion and lower levels of fatigue variables. Compared to the other groups, atypical chest pain patients were more likely to skip breakfast and showed a trend to eat fast. These findings suggest that including assessment of activity levels, fatiguability, eating behavior, neurotic traits and coronary-prone attitudes at time of coronary arteriography can have some limited value for patients with chest pain who may seek cardiac treatment but could benefit from alternative approaches.     

Chest pain and "normal" coronary arteries--role of small coronary arteries

To study the mechanism of chest pain in patients with insignificant epicardial coronary artery disease, 50 patients underwent great cardiac vein (GCV) flow, oxygen content and lactate determinations at rest and during pacing, and left ventricular end-diastolic pressure (LVEDP) measurements at rest and after pacing. Twenty-four patients having typical chest discomfort during pacing demonstrated significantly lower increase in flow from baseline (36 +/- 18% versus 86 +/- 24%, p less than 0.001) and decrease in coronary resistance (-17 +/- 12% versus -43 +/- 7%, p less than 0.001) compared with 26 patients without pacing-induced chest pain, despite no significant difference in myocardial oxygen consumption (MVO2) between the 2 groups. Lactate consumption at a heart rate (HR) of 150 beats/min was significantly less (28.3 +/- 21.5 versus 51.3 +/- 35.8 mM X ml/min, p less than 0.001) and the increase in LVEDP from rest to after pacing was significantly greater (5 +/- 2 versus 1 +/- 2 mm Hg, p less than 0.001) in the chest pain group. After administration of ergonovine, 0.15 mg intravenously, to 46 of these patients, 31 had typical pain either at rest (1 patient) or during pacing. This group had significantly lower increase in flow (38 +/- 20% versus 107 +/- 38%, p less than 0.001), and decrease in coronary resistance (-16 +/- 12% versus -45 +/- 11%, p less than 0.001) compared with the 15 patients not having chest pain, despite no significant difference in MVO2 between the 2 groups. Patients with chest pain also had lower lactate consumption at a HR of 150 beats/min (39.2 +/- 23.6 versus 65.3 +/- 46.3 mM X ml/min, p less than 0.01), greater arterial-GCV oxygen difference (12.5 +/- 1.3 versus 11.6 +/- 1.0 ml O2/100 ml, p less than 0.05), and a more marked increase in LVEDP from rest to after pacing (11 +/- 3 versus 5 +/- 2 mm Hg, p less than 0.001). Quantitative coronary arteriography demonstrated no significant luminal narrowing of the epicardial coronary arteries in response to ergonovine. These data are consistent with the hypothesis that some patients with chest pain and angiographically normal epicardial coronary arteries have dynamic abnormalities of the small coronary arteries or coronary microcirculation that cause abnormal vasodilator reserve or vasoconstriction, resulting in myocardial ischemia and angina pectoris.