摘要:

It remains unclear whether myocardial ischemia due to coronary microvascular dysfunction is the cause of chest pain in syndrome X (chest pain, ischemic-like stress ECG despite angiographically normal coronary arteries). To assess the function of the coronary microcirculation and its relation to pain perception, we measured myocardial blood flow (MBF) and coronary vasodilator reserve (CVR) in 29 patients with syndrome X and 20 matched normal control subjects.Methods and ResultsMBF at rest and after intravenous dipyridamole (0.56 mg · kg−1over 4 minutes) was measured using positron emission tomography with H215O. CVR was calculated as MBFdipyridamole/MBFrest. ECG changes and chest pain after dipyridamole in syndrome X were compared with those in 35 patients with coronary artery disease (CAD). Resting and postdipyridamole MBFs were homogeneous throughout the left ventricle in syndrome X patients and control subjects. MBF was 1.05 (0.25), mean (SD) versus 1.00 (0.22) mL. min−1. g−1(P=NS) at rest and 2.73 (0.81) versus 3.00 (1.00) mL. min−1· g−1(P=NS) after dipyridamole in patients and control subjects, respectively. CVRs were 2.66 (0.76) and 3.06 (1.08) (P=NS) and after correction of resting MBF for rate-pressure product were 2.35 (0.83) and 2.34 (0.90) (P=NS) in patients and control subjects, respectively. Female syndrome X patients had higher resting MBF than males, at 1.18 (0.20) versus 0.88 (0.19) mL min−1· g−1(P< .001). Chest pain after dipyridamole occurred in syndrome X as frequently as in CAD (21/29 versus 22/35,P=NS).ConclusionsWhen patients with syndrome X are compared with control subjects, no differences are found in MBF either at rest or after dipyridamole, despite syndrome X patients experiencing chest pain after dipyridamole to the same extent as patients with CAD. These findings, together with the absence of any relation among MBF, chest pain, and ECG changes under stress, cast further doubt on ischemia as the basis of the chest pain, at least in the majority of syndrome X patients.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

The blood coagulation system is activated in the acute phase of unstable angina and acute myocardial infarction. However, it remains unclear whether augmented function of the hemostatic mechanism serves only as a marker of the acute thrombotic episode or whether a hypercoagulable state persists for a prolonged period after clinical stabilization.Methods and ResultsWe prospectively measured the plasma concentrations of prothrombin fragment 1+2 (F1+2) and fibrinopeptide A (FPA) in consecutive patients presenting with unstable angina (n=80) or acute myocardial infarction (n=32), respectively. At 6 months, plasma determinations were repeated in patients experiencing an uneventful clinical course (unstable angina, n=57; myocardial infarction, n=23). We quantitated the plasma levels of F1+2 and FPA in control patients with stable angina (n=37) or healthy individuals (n=32) who were matched for age and sex. The median plasma concentrations of F1+2and EPA are significantly higher in patients presenting with unstable angina (F1+2, 1.08 nmol/L; FPA, 2.4 nmol/L) or acute myocardial infarction (F1+2, 1.27 nmol/L; FPA, 3.55 nmol/L) compared with patients with stable angina (F1+2, 0.74 nmol/L; FPA, 1.3 nmol/L;P< .0001) or healthy individuals (F1+2, 0.71 nmol/L; FPA, 0.80 nmol/L;P< .0001). At 6 months, the median plasma levels of F112 in patients exhibiting an uneventful clinical course did not differ from values obtained at admission (unstable angina, 1.26 versus 1.07 nmol/L,P=NS; myocardial infarction, 1.22 versus 1.29 nmol/L,P=NS), whereas the median plasma levels of FPA in the same two subpopulations were significantly reduced (unstable angina, 1.1 versus 2.9 nmol/L,P= .0003; myocardial infarction, 1.1 versus 3.0 nmol/L;P= .0028).ConclusionsDuring the acute phase of unstable angina and myocardial infarction, patients exhibit increased coagulation system activity. Over the next 6 months, patients with unstable angina or myocardial infarction experiencing an uneventful clinical course manifest a persistent hypercoagulable state with minimal generation of fibrin.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Acute closure is increased after angioplasty in unstable angina, and adjunctive intracoronary thrombolytic therapy has been used successfully to increase angiographic success. The role of prophylactic thrombolytic therapy during angioplasty in unstable angina is unknown.Methods and ResultsFour hundred sixty-nine patients with ischemic rest pain with or without a recent ( < 1 month) infarction were randomized in double-blind fashion to intracoronary urokinase or placebo. Randomization was carried out in two sequential phases. In phase I, 257 patients were randomized to 250 000 U of urokinase or placebo given in divided doses at the time of angioplasty. In phase II, 212 patients were randomized to 500 000 U of urokinase or placebo in divided doses. All patients were pretreated with aspirin, and activated clotting times were followed to maintain them at >300 seconds during angioplasty. Angiographic end points of thrombus after angioplasty were insignificantly decreased by urokinase (30 [13.8%] versus 41 [18.0%] with placebo;P=NS). Acute closure, on the other hand, was increased with urokinase (23 [10.2%] versus 10 [4.3%] with placebo;P< .02). The difference in acute closure between urokinase and placebo was more striking at the higher dose of urokinase (P< .04) than in phase I at the lower urokinase dose (P=NS). Adverse in-hospital clinical end points (ischemia, infarction, or emergency coronary artery bypass surgery) were also increased with urokinase versus placebo (30 [12.9%] versus 15 [6.3%], respectively;P< .02). Angiographic and clinical end points were worse with urokinase in unstable angina without recent infarction than with angioplasty after a recent infarction.ConclusionsAdjunctive urokinase given prophylactically during angioplasty for ischemic rest angina as administered in this trial is associated with adverse angiographic and clinical events. These detrimental effects may be related to hemorrhagic dissection, lack of intimal sealing, or procoagulant or platelet-activating effects of urokinase.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Few thrombolytic studies have assessed whether patient age is an indication for routine postlytic cardiac catheterization and revascularization or evaluated the impact of age on 1-year outcome differences after acute myocardial infarction.Methods and ResultsA secondary analysis of 3339 patients enrolled in the TIMI II trial was performed to identify differences in clinical and coronary angiographic findings and 1-year cardiac event rates among 841 patients < 50 years old, 1639 patients 50 to 64 years old, and 859 patients 65 to 75 years old. Differences in 1-year clinical outcome were assessed among patients randomly assigned to an invasive or a conservative postlytic strategy within each age group. The percentages of patients with a prior history of myocardial infarction, angina, congestive heart failure, hypertension, or diabetes mellitus or an infarction complicated at the time of study entry by shock, pulmonary edema, hypotension, rales more than one third of lung fields, or atrial fibrillation as well as the percentage of female patients (allP< .001) increased with age. Fewer older patients (65 to 75 years) received early (ie, < within 2 hours after symptom onset) treatment with recombinant tissue- type plasminogen activator (rTPA), and fewer were eligible for random assignment to immediate or deferred p-blocker therapy (P= .01). The location of the infarct-related artery and the percentage of patients with patent (ie, TIMI flow grade 2 or 3) or “omplete” (ie, TIMI flow grade 3) infarct-related artery flow did not vary with age. The percentage of patients with multivessel disease was greatest in the older patients (P= .001). Cumulative 1-year mortality was low in the youngest patients (2.8%; 99% confidence interval [CI], 1.6% to 4.7%) regardless of whether the infarct location was anterior (3.7%) or nonanterior (1.6%). The highest 1-year mortality occurred in the older patients (13.6%; 99% CI, 10.9% to 16.9%), particularly when the infarct location was anterior (18%). The 42-day rates of reinfarction (P= .85), death (P= .95), or death or reinfarction (P= .99) were similar in patients assigned to the invasive or conservative postlytic treatment strategy, regardless of age group.ConclusionsAmong patients with acute myocardial infarction treated with intravenous rTPA, heparin, and aspirin, there were age-related differences in time to treatment with thrombolytic therapy, use of β-blockers, extent of coronary artery disease, and 1-year cardiac event rates. Routine use of cardiac catheterization and coronary revascularization does not improve immediate or 1-year outcome in terms of mortality or reinfarction compared with a more conservative strategy in young, middle-aged, or elderly patients similar to those enrolled in TIMI II.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Seasonal and circadian variations in the occurrence of myocardial infarction and sudden cardiac death have been documented, suggesting that triggering factors may play a role in the causation of cardiac events. However, there are only sparse and conflicting data on the weekly distribution of the disorders.Methods and Resultsand Results To determine the weekly variation of acute myocardial infarction and sudden cardiac death, 5596 consecutive patients (71% men; age, 63±1 years) were analyzed in a regionally defined population (n=330 000; age, 25 to 74 years) monitored from 1985 to 1990. The exact time of onset of symptoms was used to determine the day of the event. Patients with myocardial infarction (n=2636) demonstrated a significant weekly variation (P< .01) with a peak on Monday, whereas patients with sudden cardiac death (n=2960) were evenly distributed throughout the week. A similar weekly pattern was observed in subgroups of patients with myocardial infarction defined with respect to age, sex, cardiac risk factors, prior cardiac medication, and infarct characteristics. The working population demonstrated a weekly variation of myocardial infarction as opposed to the nonworking population, with a 33% increase in relative risk of disease onset on Monday (P< .05) and a trough on Sunday compared with the expected number of cases, if homogeneity was assumed.ConclusionsThe onset of acute myocardial infarction demonstrates a peak on Monday primarily in the working population. If this finding is confirmed in other communities, it may aid in identifying acute triggering events of myocardial infarction and perhaps in improving prevention of the disease.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

QT dispersion (QTd, equals maximal minus minimal QT interval) on a standard ECG has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with than in those without arrhythmic events.Methods and ResultsTo assess the effect of thrombolytic therapy on QTd, we studied 244 patients (196 men; mean age, 57±10 years) with acute myocardial infarction (AMI) who were treated with streptokinase (n= 115) or anistreplase (n=129) at an average of 2.6 hours after symptom onset. Angiograms at 2.4±1 hours after thrombolytic therapy showed reperfusion (TIMI grade ≥ 2) in 75% of patients. QT was measured in 10±2 leads at 9±5 days after AMI by using a computerized analysis program interfaced with a digitizer. QTd, QRSd, JT (QT minus QRS), and JT dispersion (JTd, equals maximal minus minimal JT interval) were calculated with a computer. There were significant differences in QTd(96±31, 88±25, 60±22, and 52±19 milliseconds;P< .0001) and in JTd(97±32, 88±31, 63±23, and 58±21 milliseconds;P= .0001) but not in QRSd(25±10, 22±7, 28±9, and 24±9 milliseconds;P= .24) among perfusion grades 0, 1, 2, and 3, respectively. Similar results were obtained comparing TIMI grades 0/1 with 2/3 and 0/1/2 with 3. Patients with left anterior descending (versus right and left circumflex) coronary artery occlusion showed significantly greater QTd(70±29 versus 59±27 milliseconds,P= .003) and JTd(74±30 versus 63±27 milliseconds,P= .004). Similarly, patients with anterior (versus inferior/lateral) AMI showed significantly greater QTd(69±30 versus 59±27 milliseconds,P= .006) and JTd(73±30 versus 63±27 milliseconds,P= .007). Results did not change when Bazett's QTc, or JTc, was substituted for QT or JT or when ANOVA included adjustments for age, sex, drug assignment, infarct site, infarct vessel, and number of measurable leads. On ANCOVA, the relation of QTdor JTdand perfusion grade was not influenced by heart rate.ConclusionsSuccessful thrombolysis is associated with less QTdand JTdin post-AMI patients. The results are equally significant when either QT or JT is used for analysis. These data support the hypothesis that QTdafter AMI depends on reperfusion status as well as infarct site and size. Reduction in QTdand its corresponding risk of ventricular arrhythmia may be mechanisms of benefit of thrombolytic therapy.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Ventricular arrhythmias (VAs) are independent predictors of mortality in survivors of myocardial infarction (MI), and they are more likely to be induced in dilated hearts with increased wall stress. Angiotensin-converting enzyme (ACE)inhibitors have been shown to prevent progressive dilation of the left ventricle after MI.Methods and ResultsThe effects of captopril were evaluated in 58 patients with left ventricular (LV) dysfunction after MI. Patients were randomized on day 7 to either placebo or captopril (50 mg daily) in a double-blind parallel study over a period of 6 months. Patients were followed up by means of ambulatory ECG monitoring and echocardiography. There was a significant increase in VA in the placebo group (P< .05) in contrast to a significant decrease in the captopril group (P< .05). As a consequence, there was a significant betweengroup difference after 6 months (P< .05). Furthermore, the number of patients without VA at baseline who presented with this at the completion of the study was 6% in the captopril group versus 38% in the placebo group (P< .05). At baseline as well as at the termination of the study, LV end-diastolic volume index (LVEDVI) and LV end-systolic volume index (LVESVI) were significantly increased among patients with VAP< .01). On day 180, both myocardial ischemia and an increase in the LVEDVI were independent predictors of VA; however, progressive dilation of the left ventricle was confined to the placebo patients with significant increases in the LVEDVI compared with the captopril group: 17% versus 0%, respectively (P< .01). Furthermore, the duration of ambulatory ST-segment depression was significantly longer in this group compared with the captopril group (P< .01).ConclusionsDilation of the left ventricle and myocardial ischemia predict VA during both the acute and chronic phases after MI. In post-MI patients with LV dysfunction, captopril has a beneficial effect on both the number of complex VAs as well as the number of patients who develop VA during the chronic phase. This is in all probability mediated through effects on both LV remodeling, LV function, and myocardial ischemia in patients who are exposed to an increased risk of undergoing progressive dilation of the left ventricle.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Heart period variability provides useful prognosticinformation on autonomic cardiac control, and a strong association has been demonstrated after myocardial infarction (MI) between cardiac mortality, sudden death, and reduced total power, ultralow-frequency (ULF) power, and very-lowfrequency (VLF) power. Converting enzyme inhibitors are widely used in MI patients, but their influence on heart period variability emains to be defined.Methods and ResultsTime- and frequency-domain measures of heart period variability were calculated from 24-hour Holter monitoring in 40 patients with a first uncomplicated MI. After baseline examination between 48 and 72 hours after symptom onset, patients were randomly assigned to placebo or captopril administration, and on the third day, 24- hour Holter monitoring was repeated. No changes in time and frequency domain were detectable after placebo. After captopril, the SD of all normal RR (NN) intervals (SDNN) increased from 90±29 to 105±30 milliseconds (P< .01); the SD of the average NN intervals for all 5-minute segments (SDANN index) and the mean of the SDsof all NN intervals for all 5-minute segments (SDNN index) also increased from 74±24 to 90±26 milliseconds (P< .01) and from 45±17 to 49±15 milliseconds (P< .05), respectively. The root mean square successive difference (r-MSSD) and the percent of differences between adjacent NN intervals >50 milliseconds (pNN50) remained unchanged. In regard to frequency-domain measures, after captopril, total power (ln unit) increased from 8.28±0.42 to 8.47±0.30 (P< .01); considering the frequency bands, a significant increase was observed in ULF (P< .01), VLF (P< .05), and low-frequency (LF) power (P< .05), whereas high-frequency (HF) power remained unchanged.ConclusionsThis study supports the hypothesis that the renin-angiotensin system modulates the amplitude of ULF and VLF power. Furthermore, it demonstrates that in MI patients, converting enzyme inhibition favorably modifies measures of heart period variability strongly associated with a poor prognosis.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

This study was performed to determine the safety and potential efficacy of an intravenous perfluorochemical emulsion (Fluosol) as an adjunct reperfusion therapy aimed at preventing reperfusion injury for patients with acute myocardial infarction.Methods and ResultsPatients (430) were randomized in a prospective open-labeled study, 213 to receive Fluosol and 217 to receive no Fluosol, along with 100 mg of tissue-type plasminogen activator given over 3 hours. Major end points included global ejection fraction, regional wall motion analysis, infarct size as measured by tomographic thallium imaging, and composite clinical outcome measure. Baseline patient and angiographic characteristics were similar in the two groups. No significant difference in global ejection fraction (52% without Fluosol, 51% with Fluosol) or regional wall motion (−2.4 SD/chord with Fluosol, −2.2 SD/chord without Fluosol) was demonstrated in patients receiving Fluosol versus those not receiving Fluosol, nor was there a significant difference in thallium infarct size. Although Fluosol-treated patients with anterior infarction had an insignificantly lower mean infarct size (18.7% of the left ventricle) compared with patients with anterior infarction not treated with Fluosol (21.2% of left ventricle), this trend was not evident in the median infarct size values (22% versus 17%), left ventricular ejection fraction values (46% without Fluosol, 47% with Fluosol), or regional wall motion (−2.5 SD/chord in both groups). Rates of death and stroke were no different in the two groups; however, patients who received Fluosol experienced less recurrent ischemia. Patients receiving intravenous Fluosol had more transient congestive heart failure and pulmonary edema, perhaps because of necessary fluid administration. There was no difference in hemorrhagic complications between the two study groups.ConclusionsWhen given with a thrombolytic agent, Fluosol was not associated with improvement in ventricular systolic function, reduction in thallium infarct size, or overall clinical outcome. Fluosol was, however, associated with a reduction in ischemic complications and with an increase in pulmonary edema and congestive heart failure.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID

摘要:

Altered neural regulation of the cardiovascular system may be an important factor for various manifestations of ischemic heart disease. This research was designed to compare the circadian rhythm of cardiac neural regulation and autonomic responses to arousal and upright posture between patients with uncomplicated coronary artery disease (CAD) and age-matched subjects with no evidence of heart disease.Methods and ResultsTwenty-four-hour heart rate variability (HRV) in the frequency domain was analyzed in 20 male patients (mean age, 52±7 years) with angiographic evidence of CAD without prior myocardial infarction and in 20 healthy men (mean age, 51±8 years) with no clinical, echocardiographic, or exercise ECG evidence of heart disease. None of the 24-hour average frequency-domain components of HRV differed significantly between the two groups. Healthy subjects had a significant circadian rhythm of normalized units of high-frequency (HF) power of HRV with higher values during sleep. Normalized units of low-frequency (LF) power and the LF/HF ratio also showed a significant circadian rhythm in healthy subjects, with higher values during the daytime. No significant circadian rhythms in any of the normalized spectral components of HRV were observed in patients with CAD, and the night-day difference in LF/HF ratio was smaller in the patients with CAD than in the healthy subjects (0.5 ±1.4 versus 1.8±0.7,P< .001). Awakening when in the supine position resulted in a significant increase in the LF/HF ratio (P< .01) in the healthy subjects, but no significant changes in HRV were observed after awakening in patients with CAD. Assumption of upright position resulted in a comparable decrease in the components of HRV between the groups.ConclusionsThe circadian rhythm of cardiac neural regulation is altered in patients with uncomplicated CAD. Reduced autonomic responses to sleep-wake rhythm suggest that the modulation of cardiac autonomic function by stimuli from the central nervous system is impaired in CAD.

ISSN:0009-7322    

出版商:OVID    

年代:1994

数据来源: OVID