National Quality Measures for Breast Centers (NQMBC): a robust quality tool: breast center quality measures.

INTRODUCTION: Measuring and improving quality of care is of primary interest to patients, clinicians, and payers. The National Consortium of Breast Centers (NCBC) has created a unique program to assess and compare the quality of interdisciplinary breast care provided by breast centers across the country. METHODS: In 2005 the NCBC Quality Initiative Committee formulated their initial series of 37 measurements of breast center quality, eventually called the National Quality Measures for Breast Centers (NQMBC). Measures were derived from published literature as well as expert opinion. An interactive website was created to enter measurement data from individual breast centers and to provide customized comparison reports. Breast centers submit information using data they collect over a single month on consecutive patients. Centers can compare their results with centers of similar size and demographic or compare themselves to all centers who supplied answers for individual measures. New data may be submitted twice yearly. Serially submitted data allow centers to compare themselves over time. NQMBC random audits confirm accuracy of submitted data. Early results on several initial measures are reported here. RESULTS: Over 200 centers are currently submitting data to the NQMBC via the Internet without charge. These measures provide insight regarding timeliness of care provided by radiologists, surgeons, and pathologists. Results are expressed as the mean average, as well as 25th, 50th, and 75th percentiles for each metric. This sample of seven measures includes data from over 30,000 patients since 2005, representing a powerful database. In addition, comparison results are available every 6 months, recognizing that benchmarks may change over time. CONCLUSIONS: A real-time web-based quality improvement program facilitates breast center input, providing immediate comparisons with other centers and results serially over time. Data may be used by centers to recognize high-quality care they provide or to identify areas for quality improvement. Initial results demonstrate the power and potential of web-based tools for data collection and analysis from hundreds of centers who care for thousands of patients.

Impact of atrioventricular compliance on pulmonary artery pressure in mitral stenosis: an exercise echocardiographic study.

BACKGROUND: The decay of the pressure gradient across a stenotic mitral valve is determined by the size of the orifice and net AV compliance (C(n)). We have observed a group of symptomatic patients, usually in sinus rhythm, characterized by pulmonary hypertension (particularly during exercise) despite a relatively large mitral valve area by pressure half-time. We speculated that this discrepancy was due to low atrial compliance causing both pulmonary hypertension and a steep decay of the transmitral pressure gradient despite significant stenosis. We therefore tested the hypothesis that C(n) is an important physiological determinant of pulmonary artery pressure at rest and during exercise in mitral stenosis. METHODS AND RESULTS: Twenty patients with mitral stenosis were examined by Doppler echocardiography. C(n), calculated from the ratio of effective mitral valve area (continuity equation) and the E-wave downslope, ranged from 1.7 to 8.1 mL/mm Hg. Systolic pulmonary artery pressure (PAP) increased from 43+/-12 mm Hg at rest to 71+/-23 mm Hg (range, 40 to 110 mm Hg) during exercise. There was a particularly close correlation between C(n) and exercise PAP (r=-0.85). Patients with a low compliance were more symptomatic (P<0.025). Catheter- and Doppler-derived values for C(n), determined in 10 cases, correlated well (r=0.79). CONCLUSIONS: C(n), which can be noninvasively assessed, is an important physiological determinant of PAP in mitral stenosis. Patients with low C(n) represent an important clinical entity, with symptoms corresponding to severe increases in PAP during stress echocardiography.

Improved posterobasal segment function after thrombolysis is associated with decreased incidence of significant mitral regurgitation in a first inferior myocardial infarction.

OBJECTIVES: This study was designed to investigate the association between wall motion abnormalities and the occurrence of ischemic mitral regurgitation in patients with a first inferior or posterior myocardial infarction and to reassess the role of thrombolytic treatment in these patients. BACKGROUND: We previously demonstrated that thrombolytic therapy reduces the incidence of significant mitral regurgitation in patients with a first inferior myocardial infarction, but the mechanisms responsible for this decrease were not clear. METHODS: Wall motion score on two-dimensional echocardiography (16 segments) and mitral regurgitation grade (0 to 3) on Doppler color flow imaging were assessed in 95 patients (in 47 after thrombolysis) at 24 h, 7 to 10 days and 1 month after myocardial infarction. Significant mitral regurgitation was defined as moderate or severe (grade 2 or 3). RESULTS: Multivariate analysis revealed that the presence of an advanced wall motion abnormality of the posterobasal segment of the left ventricle was the most significant independent variable associated with significant mitral regurgitation: odds ratio (OR) 15.0, 90% confidence interval (CI) 1.4 to 165.6 at 24 h; OR 2.8, CI 0.9 to 9.3 at 7 to 10 days; OR 4.2, CI 1.2 to 11.4 at 1 month. Thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment at 24 h (55% vs. 75%, OR 0.5, CI 0.2 to 0.99), 7 to 10 days (44% vs. 73%, OR 0.3, CI 0.1 to 0.7) and 1 month (36% vs. 56%, OR 0.4, CI 0.2 to 0.9). CONCLUSIONS: There is a strong association between advanced wall motion abnormalities in the posterobasal segment and significant mitral regurgitation. In this study group, thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment and thereby reduced the incidence of significant mitral regurgitation.

Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-9: "hidden" ST-segment elevations revealing acute posterior infarction.

OBJECTIVES: This study was done to determine whether electrocardiographic (ECG) isolated ST-segment elevation (ST) in posterior chest leads can establish the diagnosis of acute posterior infarction in patients with ischemic chest pain and to describe the clinical and echocardiographic characteristics of these patients. BACKGROUND: The absence of ST on the standard 12-lead ECG in many patients with acute posterior infarction hampers the early diagnosis of these infarcts and thus may result in inadequate triage and treatment. Although 4% of all acute myocardial infarction (AMI) patients reveal the presence of isolated ST in posterior chest leads, the significance of this finding has not yet been determined. METHODS: We studied 33 consecutive patients with ischemic chest pain suggestive of AMI without ST in the standard ECG who had isolated ST in posterior chest leads V7 through V9. All patients had echocardiographic imaging within 48 h of admission, and 20 patients underwent coronary angiography. RESULTS: Acute myocardial infarction was confirmed enzymatically in all patients and on discharge ECG pathologic Q-waves appeared in leads V7 through V9 in 75% of the patients. On echocardiography, posterior wall-motion abnormality was visible in 97% of the patients, and 69% had evidence of mitral regurgitation (MR), which was moderate or severe in one-third of the patients. Four patients (12%), all with significant MR, had heart failure, and one died from free-wall rupture. The circumflex coronary artery was the infarct related artery in all catheterized patients. CONCLUSIONS: Isolated ST in leads V7 through V9 identify patients with acute posterior wall myocardial infarction. Early identification of those patients is important for adequate triage and treatment of patients with ischemic chest pain without ST on standard 12-lead ECG.

The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion.

OBJECTIVES: We sought to examine the hypothesis that rapid resolution of ST-segment elevation in acute myocardial infarction (AMI) patients with early peak creatine kinase (CK) after thrombolytic therapy differentiates among patients with early recanalization between those with and those without adequate tissue (myocardial) reperfusion. BACKGROUND: Early recanalization of the epicardial infarct-related artery (IRA) during AMI does not ensure adequate reperfusion on the myocardial level. While early peak CK after thrombolysis results from early and abrupt restoration of the coronary flow to the infarcted area, rapid ST-segment resolution, which is another clinical marker of successful reperfusion, reflects changes of the myocardial tissue itself. METHODS: We compared the clinical and the angiographic results of 162 AMI patients with early peak CK (< or =12 h) after thrombolytic therapy with (group A) and without (group B) concomitant rapid resolution of ST-segment elevation. RESULTS: Patients in groups A and B had similar patency rates of the IRA on angiography (anterior infarction: 93% vs. 93%; inferior infarction: 89% vs. 77%). Nevertheless, group A versus B patients had lower peak CK (anterior infarction: 1,083+/-585 IU/ml vs. 1,950+/-1,216, p < 0.01; and inferior infarction: 940+/-750 IU/ml vs. 1,350+/-820, p=0.18) and better left ventricular ejection fraction (anterior infarction: 49+/-8, vs. 44+/-8, p < 0.01; inferior infarction: 56+/-12 vs. 51+/-10, p=0.1). In a 2-year follow-up, group A as compared with group B patients had a lower rate of congestive heart failure (1% vs. 13%, p < 0.01) and mortality (2% vs. 13%, p < 0.01). CONCLUSIONS: Among patients in whom reperfusion appears to have taken place using an early peak CK as a marker, the coexistence of rapid resolution of ST-segment elevation further differentiates among patients with an opened culprit artery between the ones with and without adequate myocardial reperfusion.

Additional ST segment elevation during the first hour of thrombolytic therapy: an electrocardiographic sign predicting a favorable clinical outcome.

OBJECTIVES: The aim of this study was to investigate the significance of further ST elevation that occurs during the 1st h of thrombolytic therapy before the expected resolution. BACKGROUND: Early resolution of ST segment elevation is commonly accepted as a marker of clinical reperfusion during thrombolytic therapy for acute myocardial infarction. Using frequent electrocardiographic recordings, we observed in some patients further ST elevation that occurred during hour 1 of thrombolysis before the expected resolution. METHODS: To investigate the significance of this pattern, we classified 177 consecutive patients with a first acute myocardial infarction into two groups: Group A, 98 patients with ST elevation > or = 1 mm above the initial ST elevation during the 1st h of thrombolytic therapy, and Group B, 79 patients without this finding. RESULTS: Although the presence or absence of additional ST elevation was not associated with a clinical or prognostic difference in patients with a first inferior or posterior acute myocardial infarction, its presence indicated a more favorable clinical outcome and prognosis in patients with anterior infarction. Among the patients with anterior infarction the 65 patients in Group A had a higher ejection fraction (44 +/- 9% vs. 35 +/- 11%, p < 0.01), less heart failure (15% vs. 35%, p = 0.02) and a lower in-hospital mortality rate (0% vs. 8%, p = 0.04) than did the 37 patients from Group B. CONCLUSIONS: Additional ST elevation early during thrombolytic therapy in patients with anterior infarction suggests a favorable clinical outcome and thus may be indicative of successful reperfusion.

Significance of ST segment elevations in posterior chest leads (V7 to V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy.

OBJECTIVES: This study was designed to examine whether ST segment elevation in posterior chest leads (V7 to V9) during acute inferior myocardial infarction (MI) identifies patients with a concomitant posterior infarction and whether these patients might benefit more from thrombolysis. BACKGROUND: Because the posterior wall is faced by none of the 12 standard electrocardiographic (ECG) leads, the ECG diagnosis of posterior infarction is problematic and has often remained undiagnosed, especially in the acute phase. METHODS: Eighty-seven patients with a first inferior infarction who were treated with recombinant tissue-type plasminogen activator were stratified according to the presence (Group A [46 patients]) or absence (Group B [41 patients]) of concomitant ST segment elevation in posterior chest leads V7 to V9. RESULTS: Patients in Group A had a higher incidence of posterolateral wall motion abnormalities (p < 0.001) on radionuclide ventriculography, a larger infarct area (as evidenced by higher peak creatine kinase levels) (p < 0.02) and a lower left ventricular ejection fraction (LVEF) at hospital discharge (p < 0.008) than those in Group B. ST segment elevation in leads V7 to V9 was associated with a higher incidence of at least one of the following adverse clinical events: reinfarction, heart failure or death (p = 0.05). Although patency of the infarct-related artery (IRA) in Group A resulted in an improved LVEF at discharge (p < 0.012), LVEF was unchanged in Group B, regardless of the patency status of the IRA. CONCLUSIONS: ST segment elevation in leads V7 to V9 identifies patients with a larger inferior MI because of concomitant posterolateral involvement. Such patients might benefit more from thrombolytic therapy.

Underestimation of extent and severity of coronary artery disease by dipyridamole stress thallium-201 single-photon emission computed tomographic myocardial perfusion imaging in patients taking antianginal drugs.

OBJECTIVES: This study evaluated the diagnostic value of dipyridamole plus low level treadmill exercise (dipyridamole stress) thallium-201 single-photon emission computed tomography (SPECT) in patients taking antianginal drugs. BACKGROUND: Dipyridamole stress is the major substitute for maximal exercise in patients referred for myocardial perfusion imaging. Although antianginal drugs are commonly suspended before exercise, dipyridamole stress is usually performed without discontinuing these drugs. METHODS: Twenty-six patients underwent two dipyridamole perfusion studies: the first without (SPECT-1) and the second with (SPECT-2) antianginal treatment. Twenty-one patients (81%) received calcium antagonists, 19 (73%) received nitrates, and 8 (31%) received beta-blockers. Eighteen of the patients underwent coronary angiography. Data are presented as the mean value +/- SD. RESULTS: Visual scoring yielded significantly larger and more severe reversible perfusion defects for SPECT-1 than for SPECT-2. Quantitative analysis showed larger perfusion defects on stress images of SPECT-1 in the left anterior descending coronary artery (LAD) (25 +/- 21% vs. 17 +/- 15%, p = 0.003), left circumflex coronary artery (LCx) (56 +/- 35% vs. 48 +/- 36%, p = 0.03) and right coronary artery (RCA) (36 +/- 27% vs. 25 +/- 24%, p = 0.008) territories. Individual vessel sensitivities in the LAD, LCx and RCA territories were 93%, 79% and 100% for SPECT-1 and 64%, 50% and 70% for SPECT-2, respectively. These differences were highly significant for the LAD (p = 0.004) and LCx (p = 0.00004) territories. The overall individual vessel sensitivity of SPECT-1 was significantly higher than that of SPECT-2 (92% vs. 62%, p = 0.000003). Specificity was not significantly different in SPECT-1 compared with SPECT-2 (80% and 93%, p = 0.33). CONCLUSIONS: Continued use of antianginal drugs before dipyridamole plus low level treadmill exercise thallium-201 SPECT may reduce the extent and severity of myocardial perfusion defects, resulting in underestimation of coronary artery disease.

Excess mortality and morbidity associated with right bundle branch and left anterior fascicular block.

Excess mortality and morbidity associated with right bundle branch and left anterior fascicular block were evaluated in 108 patients with block (age 74 +/- 10 years, 69% male) and 108 age- and sex-matched control patients with normal conduction. Clinical characteristics were similar initially except for more congestive heart failure in patients with block. Life table analysis revealed a higher 12 year mortality with block, even after omitting patients with moderate or severe congestive heart failure (risk ratio 1.47, p less than 0.05). Compared with control subjects, the group of patients with block had more sudden death and deaths of unknown cause, but a similar number of noncardiac and diagnosed cardiac deaths. More patients with block developed new second and third degree atrioventricular block or new overt coronary artery disease, but this finding did not support prophylactic pacing in asymptomatic patients. The importance of internal controls in assessing the natural history of clinical and electrocardiographic abnormalities is emphasized.

Q wave and Non-Q wave myocardial infarction after thrombolysis.

OBJECTIVES: We studied the clinical outcome of Q wave and non-Q wave infarction after thrombolytic therapy. BACKGROUND: Controversy exists over the clinical significance of Q waves after thrombolysis. METHODS: We studied postthrombolytic angiographic results and short- and long-term clinical outcome in 150 patients with acute myocardial infarction classified as Q wave and non-Q wave on the 24-h and discharge electrocardiograms (ECGs). The results from the two groups were then compared. RESULTS: Eighty percent of patients had a Q wave and 20% a non-Q wave infarction on the 24-h ECG. The latter patients had lower peak creatine kinase (CK) levels (p < 0.001), but the two groups did not differ significantly otherwise. In 18 patients with a Q wave infarction on the 24-h ECG, pathologic Q waves disappeared. However, in seven patients with a non-Q wave infarction on the 24-h ECG, pathologic Q waves appeared throughout the hospital period. Q wave regression was associated with lower peak CK levels (p < 0.001) and an improvement in left ventricular ejection fraction (p < 0.01). Thus, only 72% of patients had a Q wave and 28% a non-Q wave infarction on the discharge ECG. Patients with a non-Q wave infarction on the discharge ECG had higher patency of the infarct-related artery (p < 0.04), lower mean peak CK levels (p < 0.0001), a higher ejection fraction (p = 0.001) and a lower incidence of heart failure (p = 0.06) than patients with a Q wave infarction on the discharge ECG. Although the 2-year incidence of reinfarction and revascularization was higher in patients with a non-Q wave infarction on the discharge ECG (p < 0.05), 2-year mortality was lower (p = 0.08). CONCLUSIONS: Although the early postthrombolytic distinction between Q wave and non-Q wave infarction conveys no significant information, during the hospital period, non-Q wave infarction is associated with a smaller infarct area, improved left ventricular function and lower mortality.

Early T wave inversion after thrombolytic therapy predicts better coronary perfusion: clinical and angiographic study.

OBJECTIVES: This study was undertaken to test the hypothesis that early inversion of T waves after thrombolytic therapy for acute myocardial infarction predicts patency of the infarct-related artery with high Thrombolysis in Myocardial Infarction (TIMI) perfusion flow and better in-hospital outcome. BACKGROUND: Although numerous studies have demonstrated a strong association between early resolution of ST segment elevation after acute myocardial infarction and successful thrombolysis, little is known about early changes in T waves after thrombolytic therapy. METHODS: Ninety-four consecutive patients with acute myocardial infarction treated with recombinant tissue-type plasminogen activator (rt-PA) were studied with admission and predischarge radionuclide ventriculography and with coronary angiography within 72 h of admission. Patient stratification was based on the presence or absence of early (within 24 h) T wave inversion. RESULTS: Early T wave inversion was associated with a higher patency rate of the infarct-related artery (90% vs. 65%, p < 0.02) and less severe residual stenosis ([mean +/- SD] 73 +/- 27 vs. 83 +/- 22, p = 0.06), and when only TIMI perfusion grade 3 was considered, the difference was even greater (77% vs. 41%, p < 0.001). Patients with early inversion of T waves had a lower peak creatine kinase value ([mean +/- SD] 678 +/- 480 vs. 1,076 +/- 620, p < 0.01), and although a similar percent of patients with and without early T wave inversion had a normal ejection fraction (> or = 55%) on admission, a higher percent of patients with early inversion had a normal ejection fraction at hospital discharge (71% vs. 44%, p < 0.03). Early T wave inversion anticipated a more benign in-hospital clinical course with a lower incidence of adverse cardiac events (10% vs. 33%, p < 0.02). CONCLUSIONS: Early inversion of T waves in patients with acute myocardial infarction treated with thrombolytic therapy suggests patency of the infarct-related artery, better perfusion grade and left ventricular function and a more benign in-hospital course.

Repeat infusion of recombinant tissue-type plasminogen activator in patients with acute myocardial infarction and early recurrent myocardial ischemia.

When conventional treatment of patients with early clinical reinfarction after thrombolytic therapy fails, mechanical revascularization may be attempted. An alternative strategy, repeat thrombolytic infusions, is reported. Fifty-two patients with acute myocardial infarction were treated with one or two additional thrombolytic infusions of recombinant tissue-type plasminogen activator (rt-PA) because of nonsustained ischemia after initial treatment with rt-PA or streptokinase. Thirty-five patients received the second infusion within 1 h of the first; 13 patients received the second infusion 1 to 72 h after the first and 4 patients received it later during their hospitalization. Bleeding complications occurred in 10 patients (19%); however, most of these were minor (no intracranial bleeding) and only 2 patients required blood transfusion. In 14 patients in whom the decrease in fibrinogen and plasminogen levels was measured after the first and second infusions, this decrease was only 25% and 63%, respectively--only slightly higher than the 22% and 53% decreases measured in 63 patients who had only one rt-PA infusion. In 44 patients (85%), the acute ischemia resolved completely within 1 h after initiation of the second infusion. In 23 patients (44%), pain and ST segment elevation did not recur and invasive coronary intervention was avoided. Thus, repeat rt-PA infusions can stabilize a substantial number of patients with acute reinfarction and, even when relief is temporary, repeat rt-PA infusions can minimize myocardial damage while patients await mechanical revascularization.

The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA.

OBJECTIVES: To determine the prevalence and clinical significance of early ST segment elevation resolution after primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (AMI). BACKGROUND: Despite angiographically successful restoration of coronary flow early during AMI, adequate myocardial reperfusion might not occur in a substantial portion of the jeopardized myocardium due to microvascular damage. This phenomenon comprises the potentially beneficial effect of early recanalization of the infarct related artery (IRA). METHODS: Included in the study were 117 consecutive patients who underwent angiographically successful [Thrombolysis in Myocardial Infarction (TIMI III)] primary PTCA. The patients were classified based on the presence or absence of reduction > or =50% in ST segment elevation in an ECG performed immediately upon return to the intensive cardiac care unit after the PTCA in comparison with ECG before the intervention. RESULTS: Eighty-nine patients (76%) had early ST segment elevation resolution (Group A) and 28 patients (24%) did not (Group B). Group A and B had similar clinical and hemodynamic features before referring to primary PTCA, as well as similar angiographic results. Despite this, ST segment elevation resolution was associated with better predischarge left ventricular ejection fraction (LVEF) (44.7 +/- 8.0 vs. 38.2 +/- 8.5, p < 0.01). Group B patients, as compared with those of Group A, had a higher incidence of in-hospital mortality (11% vs. 2%, p = 0.088), congestive heart failure (CHF) [28% vs. 19%, odds ratio (OR) = 4, 95% confidence interval (CI) 1 to 15, p = 0.04], higher long-term mortality (OR = 7.3, 95% CI 1.9 to 28, p = 0.004 with Cox proportional hazard regression analysis) and long-term CHF rate (OR = 6.5, 95% CI 1.3 to 33, p = 0.016 with logistic regression). CONCLUSIONS: Absence of early ST segment elevation resolution after angiographically successful primary PTCA identifies patients who are less likely to benefit from the early restoration of flow in the IRA, probably because of microvascular damage and subsequently less myocardial salvage.

Correlation between effects of hydralazine on force and on the adenyl cyclase system of ventricular myocardium in dogs and cats.

Hydralazine is a potent arteriolar dilator, which increases cardiac output in patients with heart failure. Previous studies suggested that these beneficial effects might be due in part to a positive inotropic effect. The present study further investigated the effect of hydralazine on myocardial contractility and adenyl cyclase activity. In isolated cat papillary muscles, bath concentrations of hydralazine up to 10(-4) mol X litre-1 did not alter force development, whereas 10(-3) mol X litre-1 hydralazine increased isometric force by 31%. This effect was blocked by 10(-6) mol X litre-1 propranolol and was absent after catecholamine depletion produced by previous reserpine treatment. In canine ventricular myocardium hydralazine in all concentrations used (10(-7) to 10(-3) mol X litre-1) increased control adenyl cyclase activity. This increase was statistically significant in 10(-6) to 10(-3) mol X litre-1 concentrations, reaching a maximum of 69.5% at 10(-4) mol X litre-1. In cat ventricular myocardium 10(-6) to 10(-3) mol X litre-1 hydralazine increased the cyclic AMP production, although to a lesser magnitude than that in canine tissue. Hydralazine 10(-5) mol X litre-1 produced a 37.8% increase, and the maximum effect of 45.2% occurred at 10(-3) mol X litre-1. The positive effects of hydralazine were completely abolished by the addition of propranolol in dogs as well as in cats. Thus the adenyl cyclase stimulation induced by hydralazine is mediated through the beta receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical profile and long-term prognosis of women < or = 50 years of age referred for coronary angiography for evaluation of chest pain.

A significant lack of information exists regarding risk factors, preventive strategies, diagnostic testing, and treatment of women with coronary artery disease (CAD), especially in the young age group. We studied the clinical profile, angiographic results, and long-term follow-up of 135 women aged < or =50 years referred for coronary angiography because of chest pain. The most prominent risk factor was hyperlipidemia (60%), followed by a family history of coronary disease (44%), systemic hypertension (40%), cigarette smoking (31%), postmenopausal state (23%), and diabetes mellitus (21%). Angiographically significant CAD was demonstrated in 79 of 135 patients (58%), most of whom (61%) had 1-vessel CAD. Women with compared to those without significant CAD had a higher prevalence of hyperlipidemia (71% vs 45%; p = 0.002) and of the post-menopausal state (30% vs 16%; p = 0.028). There was no difference in the incidence of positive noninvasive evaluation (ergometry or thallium scan) before catheterization between women with or without significant coronary lesions. At a follow-up period of 2 to 7 years, 3 women had acute myocardial infarction, all of whom demonstrated coronary lesions on prior angiography. No difference was found regarding the recurrence of chest pain on follow-up between women with or without significant CAD. Mortality and congestive heart failure were observed more frequently in women with CAD (6% vs 0%; p = 0.0516 and 12% vs 2%; p = 0.047, respectively).

Magnesium therapy in acute myocardial infarction when patients are not candidates for thrombolytic therapy.

Thrombolytic therapy reduces in-hospital mortality. However, 70% to 80% of patients do not receive thrombolysis and their in-hospital mortality is high. During the last decade some clinical trials demonstrated that magnesium sulfate reduced in-hospital mortality. The aim of this study was to evaluate the effects of magnesium sulfate in patients with acute myocardial infarction (AMI) who were considered unsuitable for thrombolytic therapy. Intravenous magnesium sulfate was evaluated in 194 patients with AMI ineligible for thrombolytic therapy in a randomized, double-blind, placebo-controlled study. Group I consisted of 96 patients who received 48-hour intravenous magnesium. Group II consisted of 98 patients who received isotonic glucose as a placebo. Magnesium reduced the incidence of arrhythmias, congestive heart failure, and conduction disturbances compared with placebo (27% vs 40%, p = 0.04; 18% vs 23%, p = 0.27; 10% vs 15%, p = 0.21, respectively). Left ventricular ejection fraction 72 hours and 1 to 2 months after admission was higher in patients who received magnesium sulfate than in those taking placebo (49% vs 43% and 52% vs 45%; p = 0.01, respectively). In-hospital mortality was significantly reduced in patients receiving magnesium sulfate than in those receiving placebo (4% vs 17%; p < 0.01), and also in the subgroup of elderly patients (> 70 years) (9% vs 23%; p = 0.09). In conclusion, magnesium sulfate should be considered as an alternative therapy to thrombolysis in patients with AMI.

Safety of pyridostigmine in hypertensive patients receiving beta blockers.

In the last decade, pyridostigmine, a quaternary carbamate that reversibly inhibits the enzyme acetylcholinesterase, was proposed for pretreatment of nerve gas (organophosphate) poisoning. The objective of this study was to assess the cardiovascular effects of pyridostigmine in patients treated with beta blockers. Eight hypertensive patients receiving regular treatment with beta blockers were randomized in a double-blind crossover study to receive pyridostigmine (30 mg 3 times daily) or placebo for 2 days. Heart rate and blood pressure in the supine and standing positions were recorded every 2 hours during the day, and 24-hour Holter monitoring was performed. In addition, a symptom-limited exercise test was performed, and plasma catecholamine levels were determined at rest and at peak exercise. Pyridostigmine, as compared with placebo, did not induce any significant effect on heart rate, plasma catecholamine levels or resting blood pressure. Both systolic and diastolic blood pressures increased in accordance with exercise intensity (p less than 0.01), although a significantly lower diastolic blood pressure was observed when pyridostigmine was used (average decrease 5 mm Hg compared with placebo; p less than 0.01). No clinical adverse reactions were observed, confirming the relative safety of the combination of low-dose pyridostigmine with beta-adrenergic blocking agents.

Beneficial effect of magnesium sulfate in acute myocardial infarction.

The effects of magnesium on the incidence of arrhythmias and on mortality were evaluated in 103 patients with documented acute myocardial infarction (AMI) in a randomized, double-blind, placebo-controlled study. Fifty patients received a magnesium infusion for 48 hours and 53 received only the vehicle (isotonic glucose) as placebo. The baseline characteristics of the population were similar in the 2 groups. Tachyarrhythmias requiring drug therapy were recorded in 32% of the patients in the magnesium group and in 45% of the placebo group. Conduction disturbances were found in 23% of the placebo group as compared to 14% in the magnesium group. The intrahospital mortality was 2% (1 patient) in the magnesium group, compared to 17% (9 patients) in the placebo group (p less than 0.01). No adverse effects were observed during and after the magnesium infusion. These data support a possible protective role of magnesium in patients with AMI.

Immediate and long-term prognostic significance of a first anterior versus first inferior wall Q-wave acute myocardial infarction. Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) Study Group.

Of 3,981 patients with a first Q-wave acute myocardial infarction (AMI), 1,929 (48%) had an anterior and 1,724 (43%) an inferior wall AMI. These 2 groups were well-matched with respect to age, gender and relevant history. The in-hospital mortality rate was 18%, and the 1- and 5-year post-discharge mortality rates were 9 and 25%, respectively, in patients with anterior wall AMI compared with the corresponding rates of 11, 6 and 19% in those with inferior wall AMI (p < 0.0001 for each category). The frequency of recurrent nonfatal AMI in the year after the index AMI was 8% in the patients with anterior wall AMI compared with 4% in those with inferior wall AMI (p < 0.0001). By multiple logistic regression analysis of events, anterior wall AMI was an independent predictor of in-hospital mortality only. The findings indicate that the anatomic location of a Q-wave AMI influences immediate and short-term survival of patients with a first Q-wave AMI.

Frequency and prognostic significance of secondary ventricular fibrillation complicating acute myocardial infarction. SPRINT Study Group.

The incidence of secondary ventricular fibrillation (VF) complicating acute myocardial infarction (AMI) was 2.4% in a large cohort of unselected patients with AMI (142 of 5,839). Secondary VF was more frequent in patients with recurrent AMI (4%) than in those with a first AMI (1.9%) (p < 0.01). The hospital course was more complicated and in-hospital mortality was significantly higher in patients with secondary VF than in those with the same clinical hemodynamic condition but without VF (56 vs 16%; p < 0.0001). Multivariate analyses confirmed secondary VF complicating AMI as an independent predictor of high in-hospital mortality, with an odds ratio of 7 (95% confidence interval 4.6-10.6). However, long-term mortality after discharge (mean follow-up 5.5 years) was not increased in patients with as compared with those without secondary VF (39 vs 42%). These findings were also true when patients receiving beta blockers and antiarrhythmic therapy were excluded from analysis. Thus, this life-threatening arrhythmia occurring during hospitalization is not a marker of recurrent susceptibility to VF or an indicator of increased mortality after discharge from the hospital.