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Biomedical subjects

S Ben Freedman

Publications and source records attributed to S Ben Freedman.

12 recordsLinked to original sources
PubMed2007

High risk-factor level and low risk-factor knowledge in patients not accessing cardiac rehabilitation after acute coronary syndrome.

OBJECTIVE: To document the risk-factor profile and risk-factor knowledge of patients with an acute coronary syndrome (ACS) not attending standard cardiac rehabilitation. DESIGN AND SETTING: Cross-sectional comparison in a tertiary hospital. PARTICIPANTS: Patients admitted to hospital with an ACS, residing within 20 km of the hospital, and without severe comorbidity who did not access cardiac rehabilitation (NCR) were compared with a group about to commence standard cardiac rehabilitation (SCR). MAIN OUTCOME MEASURES: Risk-factor profile, knowledge of risk factors via face-to-face assessment, quality of life. RESULTS: Of the 446 patients eligible for cardiac rehabilitation, 208 attended for assessment (NCR: n = 144; SCR: n = 64). The NCR group had higher mean (+/- SEM) low-density lipoprotein (LDL) cholesterol levels (2.6 +/- 0.1 v 2.3 +/- 0.1; P = 0.02), and were more likely than the SCR group to have a total cholesterol level of > 4.0 mmol/L (78% v 53%; P < 0.001) and an LDL cholesterol level > 2.5 mmol/L (47% v 25%; P = 0.01). They were more likely than the SCR group to be physically inactive (77% v 22%; P < 0.001); obese (46% v 33%; P = 0.04); depressed (21% v 5%; P < 0.001); or current smokers (21% v 1%; P < 0.001). Compared with the SCR group, the NCR group also had higher risk scores (LIPID risk score) (4.5 v 2.1; P < 0.001); lower quality of life (Medical Outcome Short Form [SF-36] Health Survey); and significantly poorer knowledge of risk factors. Among patients with at least two modifiable cardiac risk factors, the NCR group were less likely than the SCR group to be able to state at least one risk factor (24% v 38%; P < 0.001). CONCLUSIONS: Patients not participating in cardiac rehabilitation after an ACS have more adverse risk profiles and poorer knowledge of risk factors compared with those about to commence cardiac rehabilitation. Alternate models for secondary prevention are required to improve health outcomes in patients not attending cardiac rehabilitation.

Adult↗
PubMed2005

The role of left ventricular hypertrophy and diabetes in the presence of transient ischemic dilation of the left ventricle on myocardial perfusion SPECT images.

UNLABELLED: Transient ischemic dilation of the left ventricle found on SPECT myocardial perfusion imaging (MPI) is an accepted marker of severe and extensive coronary artery disease (CAD) and poor prognosis. The influence of other clinical variables on the incidence of transient ischemic dilation is less certain. The aim of this study was to investigate clinical factors that may influence the incidence of transient ischemic dilation. In particular, we looked at factors that may independently affect subendocardial perfusion, such as left ventricular hypertrophy (LVH) and diabetes. METHODS: MPI studies of 103 consecutive patients who had undergone recent coronary angiography (< or =6 mo) and transthoracic echocardiography within a year of stress electrocardiography-gated MPI were retrospectively analyzed. Transient ischemic dilation was assessed quantitatively using a software program. A ratio cutoff of > or =1.22 was considered to represent transient ischemic dilation. Summed stress score and summed difference score (ischemia score) were determined using the standard 17-segment 5-point scoring system to quantify myocardial ischemia. LVH was defined as a left ventricular wall thickness of >11 mm on M-mode echocardiography. Severe CAD was defined as severe stenosis (> or =90%) of either the left anterior descending artery or both the right coronary and lateral circumflex arteries. RESULTS: Nineteen (18%) of the 103 patients had transient ischemic dilation, 19 (18%) had LVH, and 23 (22%) were diabetic. A high percentage had severe CAD (46/103 [45%]), whereas 57 of 103 (55%) had less severe CAD (30/103 [29%]) or nonsignificant CAD (26/103 [25%]). Severe CAD (P < 0.001), diabetes (P < 0.0001), LVH (P < 0.003), and the ischemia score (P < 0.023) were independent predictors of transient ischemic dilation by multivariate logistic regression. In patients with severe CAD, the effect of LVH on the incidence of transient ischemic dilation was additive, increasing the incidence from 21% (8/38) without LVH to 75% (6/8) with LVH (P < 0.006). Likewise, with severe CAD, the incidence of transient ischemic dilation rose from 21% (7/33) in patients without diabetes to 54% (7/13) in those with diabetes (P < 0.04). CONCLUSION: The presence of transient ischemic dilation on myocardial perfusion SPECT is associated with the presence of severe CAD, but this association is modified by the presence of LVH and diabetes.

Aged↗
PubMed2003

Effects of angiotensin-converting enzyme inhibition on transient ischemia: the Quinapril Anti-Ischemia and Symptoms of Angina Reduction (QUASAR) trial.

OBJECTIVES: We sought to determine whether angiotensin-converting enzyme inhibition (ACE-I) (i.e., quinapril) prevents transient ischemia (exertional and spontaneous) in patients with coronary artery disease (CAD). BACKGROUND: It is known that ACE-I reduces the risk of death, myocardial infarction (MI), and other CAD-related outcomes in high-risk patients. Numerous studies have confirmed that ACE-I improves coronary flow and endothelial function. Whether ACE-I also decreases transient ischemia is unclear, because no studies have been adequately designed or sufficiently powered to evaluate this issue. METHODS: Using a randomized, double-blinded, placebo-controlled, multicenter design, we enrolled 336 CAD patients with stable angina. None had uncontrolled hypertension, left ventricular (LV) dysfunction, or recent MI, and all developed electrocardiographic (ECG) evidence of ischemia during exercise. They were randomly assigned to one of two groups: 40 mg/day quinapril (n = 177) or placebo (n = 159) for 8 weeks. Patients then entered an additional eight-week treatment phase to examine the full dose range. Those assigned to 40 mg quinapril continued that dose and those assigned to placebo were titrated to 80 mg/day. Treadmill testing, the Seattle Angina Questionnaire, and ambulatory ECG monitoring were used to assess responses at baseline and at 8 and 16 weeks. RESULTS: The groups did not differ significantly at entry or in terms of indexes assessing myocardial ischemia at 8 or 16 weeks of treatment. In this low-risk population, ACE-I was not associated with serious adverse events. CONCLUSIONS: Our findings suggest short-term ACE-I in CAD patients without hypertension, LV dysfunction, or acute MI is not associated with significant effects on transient ischemia.

Angina Pectoris↗
PubMed2002

Optimal strategy for administering enoxaparin to patients undergoing coronary angiography without angioplasty for acute coronary syndromes.

The optimal strategy for administration of low molecular weight heparin in patients with acute coronary syndrome (ACS) undergoing coronary angiography without percutaneous coronary intervention remains unclear. We studied postangiographic vascular complications in 325 consecutive patients (210 men and 115 women, mean age 63 years) with ACS undergoing diagnostic coronary angiography via a femoral approach followed by immediate sheath removal. At the time of angiography, 44 patients were on intravenous unfractionated heparin (UFH), 229 on subcutaneous enoxaparin, and 52 on no heparin. Enoxaparin was withheld on the morning of angiography in 181 of 229 patients: the no A.M. dose group. Vascular complications were audited, including hematoma development at angiographic puncture sites; these complications were considered significant if >25 cm(2). Major vascular complications requiring transfusion or surgical interventions were infrequent in all groups. Patients receiving enoxaparin on the morning of angiography had a twofold increase in significant hematoma rate compared with the no A.M. dose group (31% vs 16%; p = 0.015). The no A.M. dose group had hematoma rates similar to UFH (20%; p = NS) and no anticoagulation (13.5%; p = NS). No significant increase in ischemic episodes occurred as a result of withholding enoxaparin in the no A.M. dose group. We conclude that omission of enoxaparin on the morning of cardiac catheterization results in vascular complications rates comparable to that of UFH without precipitating rebound ischemia. This is a practical, safe strategy for patients with ACS undergoing coronary angiography, allowing early mobilization for most patients who do not proceed to immediate percutaneous coronary intervention.

Acute Disease↗
PubMed1999

Vascular risk factors correlate to the extent as well as the severity of coronary atherosclerosis.

BACKGROUND: Because most acute coronary events result from thrombosis at sites of minor plaque, the extent of non-obstructive coronary artery disease (CAD), rather than simply the number of severe stenoses, might be clinically relevant. OBJECTIVE: To examine the relationship between vascular risk factors and a novel extent score for CAD that measures the percentage of the coronary tree involved with atheromatous plaque, as judged by coronary angiography. METHODS: We assessed the extent and severity of CAD and the presence of vascular risk factors of 429 consecutive eligible patients (296 men, aged 61 +/- 11 years) who presented for elective coronary angiography. Detailed analyses of lipid levels were performed for 126 subjects. RESULTS: The mean extent score was 54 (range 0-100). The presence of diabetes (P < 0.001), current or former smoking (P < 0.005) and a history of hypertension (P < 0.001) were all strongly associated with the CAD extent score, as was severity of disease. For the 283 patients with one or no severe stenosis, diabetes was associated with a greater extent score (57 versus 41%, P < 0.005), as was smoking (49 versus 34%, P < 0.005). For the 126 patients with detailed data on lipid levels, extent of coronary artery disease was independently correlated to age (P < 0.005), male sex (P < 0.05), presence of diabetes (P < 0.05), hypertension (P < 0.05), level of lipoprotein (a) (P < 0.005) and low-density:high-density lipoprotein ratio (P < 0.01) in multivariable analysis. CONCLUSIONS: Extent of CAD, as well as its severity, is significantly associated with traditional vascular risk factors. Because most acute coronary events occur at sites of minor plaque, this might explain the mechanism whereby risk factors confer adverse prognostic significance.

Coronary Artery Disease↗
PubMed1990

ST monitoring for myocardial ischemia during and after coronary angioplasty.

We performed 12-lead electrocardiographic monitoring in 97 patients during coronary angioplasty (PTCA) of a single vessel to correlate ischemic ST changes with clinical, angiographic and coronary hemodynamic variables and to determine the optimum lead or combination of leads for their detection. Ischemia (chest pain or ST change, group A) occurred in 79 patients (80%), but in only 15 of 23 patients (65%) with collaterals (p less than 0.05). Ischemia occurred more often in left anterior descending and left circumflex PTCA than right coronary PTCA, but pain was the only manifestation more often in left circumflex and right coronary PTCA. Ischemic ST change was silent in 16% and this proportion did not differ in clinical or angiographic groups except for diabetes with 3 of 5 (60%) having silent ischemia (p less than 0.05). Patients in group A (ischemia) compared to group B (no ischemia) had less severe lesions (85 +/- 9 vs 91 +/- 7%, p less than 0.01), higher transstenotic gradients (62 +/- 19 vs 53 +/- 9 mm Hg, p less than 0.05) and lower distal occluded pressures (24 +/- 11 vs 33 +/- 10 mm Hg, p less than 0.01), suggesting less collateral flow. Compared with a 12-lead electrocardiogram, the best single lead for detecting ST change during PTCA in each artery had a sensitivity of 80% and this increased to 93% using the best 2 leads. The best 3 leads (V3/III/V5 for left anterior descending and III/V2/V5 for right coronary and left circumflex) increased sensitivity to 100%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

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.

Angina Pectoris↗
PubMed1987

Validation of a real-time electrocardiographic monitor for detection of myocardial ischemia secondary to coronary artery disease.

A new real-time electrocardiographic (ECG) monitor (QMED Monitor OneTM) was evaluated to assess its accuracy in detecting ischemic ST-segment changes in 43 patients (34 men, 9 women, mean age 56 +/- 11 years) during exercise stress testing. The output of QMED was compared with ST-segment measurements from a Marquette CASE-II computer (ECGM) using a bipolar lead CM5, defining a positive ECG as at least 1 mm of planar or downsloping ST depression. Results were concordant in 33 patients, 15 with both positive and 18 both negative responses, yielding an accuracy (expressed as sensitivity, specificity, positive and negative predictive accuracy) of 83%, 72%, 68% and 86%, respectively. Seven false-positive QMED episodes occurred: 4 due to excess baseline wander or noise in the control ECG, which may have been prevented by reapplication of electrodes, and all 7 episodes were correctly discounted by inspection of the sample ischemic ECG output, yielding an accuracy of 81%, 100%, 100% and 85%. Mean duration and maximal magnitude of ST depression in patients with a positive ECG response was 7.9 +/- 7 minutes and 1.7 +/- 0.6 mm for QMED and 8.9 +/- 7 minutes and 2.2 +/- 0.7 mm for ECGM. The 3 false-negative QMED events were relatively brief and mild ischemic episodes and slight differences in electrode placement between the 2 systems may account for this discrepancy in 2 of the patients. Real-time ST monitoring with QMED is sufficiently reliable for clinical use. Optimal specificity depends on the ability to inspect sample ECG traces to verify a stable baseline and confirm episodes of ischemic ST-segment shift.

Coronary Disease↗