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Biomedical subjects

J E Calvin

Publications and source records attributed to J E Calvin.

At least 37 records · Page 2Linked to original sources
PubMed1997

Comparison of heparin therapy for < or = 48 hours to > 48 hours in unstable angina pectoris.

Of 450 consecutive patients with unstable angina admitted to a tertiary care, university-based medical center over a 24-month period, 334 were administered heparin and aspirin for some length of time. Two groups of 98 patients matched for acuity and gender at baseline were treated with either < or = 48 hours (group 1) or > 48 hours (group 2) of heparin. The acuity model used in this study incorporates 6 factors: age, recent myocardial infarction, treatment with intravenous nitroglycerin, previous therapy with beta blockers or calcium antagonists, baseline ST depression, and diabetes. Despite similar risks and overall clinical outcome, group 2 had significantly more myocardial infarction or death after 48 hours than group 1 (p = 0.01). In part, this was due to a delay in the performance of coronary angiography (2.8 +/- 1.4 vs 3.5 +/- 15 days, p = 0.01), coronary intervention (2.7 +/- 1.8 vs 5.1 +/- 2.3 days, p = 0.01), and bypass surgery (3.8 +/- 3.6 vs 7.0 +/- 5.6 days, p = 0.02). There was no difference between groups regarding the success of coronary intervention (90% vs 88%, p = NS). Heparin duration was influenced by the finding of intracoronary thrombus or ulceration on angiography before revascularization, as each finding was seen more often in group 2 (thrombus, 12% vs 24%; ulceration, 38% vs 60%). These results suggest that the optimal duration of heparin therapy is up to 48 hours after admission in unstable angina; a longer time period is associated with increased adverse consequences.

Aged↗
PubMed1997

Does low individual operator coronary interventional procedural volume correlate with worse institutional procedural outcome?

OBJECTIVES: To assess the relation between individual operator coronary interventional volume and incidence of complications, the in-hospital outcome at a single, moderate volume urban academic center was prospectively collected over a 3-year period. BACKGROUND: A minimum of 75 coronary interventions/operator per year may be required in the future to obtain formal certification. However, few data exist regarding individual operator volumes and procedural outcome. METHODS: Between January 1993 and December 1995, 1,389 consecutive procedures were performed or supervised by nine geographic full-time operators: 171 (12.3%) utilized various devices, and 350 (25.2%) involved multivessel coronary intervention. Left ventricular ejection fraction was 59 +/- 15% (mean +/- SD), and there were 1.7 +/- 0.7 vessels diseased (with > or = 70% stenosis). Clinical indications included stable angina in 22.5% of cases, unstable angina in 31.9%, acute myocardial infarction (MI) in 2.9%, post MI in 20.6%, shock or acute heart failure in 3.0% and restenosis in 19.1%. In the last consecutive 857 lesions in 655 cases, 20.7% type A, 55.5% type B and 23.8% type C lesions were categorized before coronary intervention. RESULTS: Average yearly operator volume ranged from 26 to 83 cases (mean 51 +/- 26). Each operator has performed a total of 590 +/- 268 coronary interventions, with 10.0 +/- 4.3 years of coronary interventional experience. The mean angioplasty volume rating for the nine operators was 180 +/- 37 (> 170 considered adequate). The in-hospital major complication rate was 1.4% (95% confidence interval 0.7% to 1.893%) for all coronary interventions, including death in 3 patients, bypass surgery in 13, arrhythmia in 3 and Q wave MI in 2. To ascertain how these outcomes compared with standard measures of coronary interventional outcome, four previously published registries were reanalyzed in a similar manner. The rate of complications in the present study was found to be significantly lower than that of the 1992-1993 Society for Cardiac Angiography and Intervention registry (1.9%, n = 19,594, p < 0.05 [excludes ventricular arrhythmias]), the 1994 American College of Cardiology database (3.9%, n = 38,963, p = 0.001), the Mid-America Heart Institute outcome in 1988 (2.3%, n = 5,413, p = 0.02) and the 1985-1986 National Heart, Lung, and Blood Institute Registry (7.2%, n = 1,801, p = 0.001). Odds ratios and 95% confidence intervals showed the outcome in the current study to be at least comparable to the standard registries. CONCLUSIONS: Despite individual operator volumes below those currently being considered for credentialing, the overall institutional outcome was excellent in a diverse and complex patient population.

Academic Medical Centers↗
PubMed1997

Critical care in the United States. Who are we and how did we get here?

Critical care medicine has progressed significantly over the past two to three decades. We will review the history and evolution of critical care medicine and ICUs in the United States. The evolving health care delivery system and the changing and important role of the intensivist will be addressed. Finally, a discussion about what critical care physicians must do to prepare for the future is presented.

Critical Care↗
PubMed1997

Pulmonary artery catheterization: a narrative and systematic critique of randomized controlled trials and recommendations for the future.

OBJECTIVE: The purpose of this review is to evaluate the current literature regarding the efficacy of pulmonary artery catheterization, to assess the quality of existing randomized controlled trials and to make recommendations for future studies. DATA SOURCE: A Medline search was conducted of English language studies published between 1970 and 1996 using as search terms "Swan-Ganz catheterization," "pulmonary artery catheterization," and "right heart catheterization." STUDY SELECTION: Randomized controlled trials of pulmonary artery catheterization were selected for review. Sixteen randomized controlled trials were identified. DATA EXTRACTION: The quality of the randomized controlled trials was assessed and a formal meta-analysis was performed. DATA SYNTHESIS: The overall quality score was 40.15 +/- 6.32 out of a possible score of 100. Serious deficiencies were identified including a lack of a priori sample size calculations, unclear definitions of concomitant therapy, inability to blind physicians and patients, and lack of blinded outcome assessments. A random effects model found the relative risk ratio of .808 (95% confidence interval [CI] = .598, 1.091; p = .148). An analysis of potential covariates revealed patients from surgical series treated with pulmonary artery catheter (PAC)-guided therapy had a relative risk ratio of .578 (95% CI = .357, .937; p = .03) compared with control groups. Patients from medical or mixed unit series had a relative risk of 1.043 (95% CI = .784, 1.387; p = NS). CONCLUSION: Existing randomized controlled trials on PAC-guided strategies reveal a modest risk reduction that does reach statistical significance. Risk reduction appears to be greatest in surgical series. Deficiencies of these trials have important implications for the proper design of future trials.

Catheterization, Swan-Ganz↗
PubMed1995

Utility of various clinical, noninvasive, and invasive procedures for determining the causes of recurrence of myocardial ischemia or infarction > or = 1 year after percutaneous transluminal coronary angioplasty.

In patients with recurrent symptoms > or = 1 year after successful percutaneous transluminal coronary angioplasty (PTCA), the decision of whether to proceed directly with coronary angiography or to evaluate the patient noninvasively can be difficult. To determine which demographic, historical, clinical, and laboratory factors are useful in helping to make this decision, 76 consecutive patients who presented > 1 year (768 +/- 309 days) after successful PTCA with resolution of symptoms were studied. The initial PTCA successfully treated all stenoses (except chronically occluded vessels) in all major vessels and segments. The patient group was predominantly men (68%), with a mean age of 64 +/- 10 years. A prior myocardial infarction was present in 39 patients (51%), and there was a mean of 2.8 risk factors per patient. In patients who presented with recurrent symptoms, the Canadian Cardiovascular Society functional class was 2.0 +/- 0.9; 2 patients presented with acute infarctions, 57 were admitted to the hospital with unstable angina, and 17 had stable angina. New electrocardiographic changes at rest were found in 19 of 74 patients (26%) with recurrent angina. A thallium stress test was performed in 40 patients (53%), with a sensitivity of 77% and a specificity of 36% for the presence of a significant stenosis. No nonangiographic variable was predictive of angiographic findings. At angiography, the number of coronary arteries with > or = 50% diameter narrowing was 1.4 +/- 1.0. Forty-two patients had stenosis at a new site, 7 had restenosis, and 27 had no new stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Risk stratification in unstable angina. Prospective validation of the Braunwald classification.

OBJECTIVES: To validate the Braunwald classification of unstable angina as a predictor of in-hospital cardiac complications; to determine which factors of the Braunwald classification contributed significantly to this prediction; and to devise a method of combining these predictive factors into an overall odds ratio for complications. DESIGN: A validation cohort of consecutive patients followed prospectively for in-hospital cardiac complications including myocardial infarction and death. SETTING: A community-based academic medical center. PATIENTS: A total of 393 patients admitted consecutively to the coronary care and intermediate care units with unstable angina. MAIN OUTCOME MEASURES: Major cardiac complications including death, myocardial infarction, congestive heart failure, cardiogenic shock, and severe ventricular dysrhythmias. RESULTS: Multiple logistic regression analysis identified four clinical factors used in the Braunwald classification that predicted the in-hospital occurrence of major cardiac complications: (1) myocardial infarction within less than 14 days (odds ratio [OR], 5.72; 95% confidence interval [CI], 1.92 to 16.97); (2) need for intravenous nitroglycerin (OR, 2.33; 95% CI, 1.31 to 4.17); (3) lack of beta-blocker or calcium channel blocker prior to admission (OR, 3.83; 95% CI, 1.55 to 9.42); and (4) baseline ST depression (OR, 2.81; 95% CI, 1.45 to 5.47). Two other clinical factors, diabetes and age, were also significant predictors. Validation of this model using parametric and nonparametric bootstrap techniques revealed excellent agreement between the CIs for adjusted ORs derived from the multiple logistic regression and those derived from the bootstrap. CONCLUSIONS: The classification of unstable angina proposed by Braunwald includes four factors that predict risk of major in-hospital cardiac complications. Specific factors used in this classification can be combined with diabetes and age to better stratify risk of major cardiac complications in this disorder using a simpler model.

Age Factors↗
PubMed1995

Circadian variations in cardiac disease: clinical implications. Current strategies for preventing MI, dysrhythmias, sudden death.

Myocardial infarction (MI), myocardial ischemia, ventricular dysrhythmias, and sudden cardiac death (SCD) occur most frequently in the morning, especially in the first few hours after awakening. Among individual patients, however, this pattern may vary widely. Peaks in heart rate, blood pressure, and platelet aggregability and a trough in fibrinolytic activity are thought to influence the morning onset of events. beta-Blockers may blunt the peak occurrence of MI, SCD, and ischemia. Some calcium channel blockers may modify the pattern of ischemia. Alternate-day therapy with 325 mg of aspirin has been shown to blunt the morning onset of MI. The efficacy of thrombolytics may be affected by daily fluctuations in fibrinolytic activity.

Arrhythmias, Cardiac↗
PubMed1994

Does septal position affect right ventricular function during left ventricular assist in an experimental porcine model?

Right ventricular (RV) failure has been a major problem with patients supported by left ventricular (LV) assist devices (LVADs). To assess the importance of interventricular septal (IVS) position as a mechanism of RV failure, 7 Yorkshire pigs underwent implantation of a Thoratec LVAD. RV function was assessed before and during LVAD operation under differing conditions: (1) with an LV intraventricular latex balloon inflated or deflated to alter IVS position and (2) with and without pulmonary artery (PA) constriction to assess the effect of changes in afterload. RV stroke work, RV dP/dt, and RV end-diastolic length did not change significantly with LVAD operation or with changing afterload conditions. Septal shift was documented as a change in LV shape index (LVSI) calculated using echocardiography. LVSI decreased by 11% when the LVAD was turned on, indicating leftward shifting of the IVS (P = .01). During LVAD support and increased RV afterload, the LVSI decreased by 14.8% (P = .02). RV cardiac output decreased somewhat during LVAD support. However, RV output was worst when the septal position was normalized using the inflated intraventricular balloon during increased RV afterload (P = .05). Unloading by the LVAD of the left ventricle results in a leftward shift of the interventricular septum, which does not appear to adversely affect RV function. However, during conditions of increased RV afterload, septal shifting may be beneficial to RV function.

Animals↗
PubMed1993

Pulmonary artery catheterization. Can there be an integrated strategy for guideline development and research promotion?

OBJECTIVES: To review the evidence regarding indications for pulmonary artery catheterization (PAC) in critically ill patients, and to propose a guideline-generating process that would encourage randomized controlled trials of PAC. DATA SOURCES: Computerized and manual search for randomized trials involving PAC as an integral part of the protocol, published as of October 1992. Manual search for guidelines endorsed by specialty societies and/or proposed by expert panels following an explicit group process. DATA SYNTHESIS: Four trials suggest benefit from PAC for pre- or perioperative management of high-risk surgical patients. Two others indicate that PAC for low-risk aortic aneurysm surgery confers no advantages. Use of PAC to guide therapy aimed at improved mixed venous oxygen saturation was beneficial compared with usual care with PAC in two small trials among patients with septic shock and severe trauma. Other PAC indications are either untested or inadequately tested by small trials. Large trials are needed, but trials to date have been impeded by clinicians' uncertainty about PAC and unwillingness to randomize critically ill patients. No published guidelines for PAC have used a formal group process and/or a hierarchical review of evidence to demarcate proven from unproven indications. CONCLUSIONS: We propose a research-promoting expert panel on indications for PAC. Aided by a critical literature review, experts would rate case scenarios on the need for routine PAC with or without a specified intervention strategy. Future trials should test indications where there is either consensus about the uncertainty of need for PAC, or interpanelist disagreement owing to inconclusive evidence. This process could facilitate practice guideline development, utilization management, and large trials of PAC and related interventions.

Cardiac Catheterization↗
PubMed1993

A survey of charting in critical care units.

OBJECTIVES: To determine what data are currently being collected at the critical care bedside, the role of flow sheets in storing these data, and what other forms and locations are used to store critical care data. DESIGN: We undertook a descriptive survey in a nonrandom sample of acute care hospitals with designated critical care units. Flow sheets were reviewed, and interviews with critical care nurses and physicians were conducted according to a predefined questionnaire. Finally, compliance in the surveyed hospitals with previous recommendations and existing guidelines on data collection and storage was then determined. SETTING: Fifteen "teaching" and 19 "nonteaching" acute care hospitals in the Province of Ontario. RESULTS: A lack of standardization of flow-sheet design and of the specific data included on these flow sheets was identified. Abbreviations were inconsistent. Little collaboration between physician and nonphysician members of the critical care team was identified in flow-sheet design. Variance between units in their collection of physiologic data was remarkable. Finally, few units surveyed used quantifiable illness severity scoring to describe their unit population. CONCLUSIONS: The lack of standardization regarding key information that should be collected and archived in critical care units identifies important risk management and quality assurance issues. There is a need for agreement on what information should be collected and maintained at the bedside in order to provide quality patient care.

Critical Care↗
PubMed1991

Pressure segment length analysis of right ventricular function: influence of loading conditions.

The purpose of this study was to determine whether segment lengths measured from the right ventricular inflow and outflow tract regions of the right ventricle would accurately reflect true volume changes of the right ventricle and to determine the response of the right ventricle to afterload increases induced by both constricting the pulmonary artery (PAC) and embolizing the pulmonary circulation with glass beads (GBE). Three excised hearts were instrumented with segment-length crystals attached to the inflow and outflow tract regions, and saline was instilled into a balloon implanted inside the right ventricular cavity. The experiments showed a high correlation (r greater than or equal to 0.90 in all cases) between static segment lengths and volume instilled. In open chest, open pericardial canine experiments, vena caval occlusion reduced end-diastolic segments lengths and right ventricular systolic pressure consistent with a reduction in right ventricular end-diastolic volume. In a separate group of animals, volume loading with dextran increased inflow and outflow end-diastolic segment lengths and increased cardiac output. In two further groups of animals, one of which was pretreated intravenously with propranolol (Inderal), both forms of pressure overload increased end-diastolic lengths in both regions. However, GBE increased right ventricular stroke work compared with PAC. We conclude that end-diastolic segment lengths reflect true volume changes of the right ventricle. Furthermore, during acute pressure overload, the right ventricle dilates to compensate for the afterload change. However, ventricular function is better maintained after GBE.

Animals↗
PubMed1991

Optimal right ventricular filling pressures and the role of pericardial constraint in right ventricular infarction in dogs.

BACKGROUND: Previous studies have reported an important role for right ventricular function in the pathophysiology of the low cardiac output state that can accompany right ventricular infarction. Some studies have suggested that right ventricular distensibility impairs right ventricular filling and stroke output; others have demonstrated that the pericardium can mediate depressed left ventricular filling and stroke output. METHODS AND RESULTS: To determine the role of pericardial constraint and optimal volume loading in an experimental model of right ventricular wall infarction, six mongrel dogs were studied before and after right ventricular wall infarction and after volume loading. The pericardium was then opened in two phases. In the first phase, the pericardium was opened partially to allow the atria to distend freely, and in the second phase, the pericardium was opened completely. The animals were preinstrumented with two sets of piezoelectric crystals attached to the right ventricular free wall, one in the infarct and the other in the noninfarct territory. Left ventricular size was estimated by left ventricular crystals on the anterior wall of the left ventricle. Right ventricular and left ventricular Millar catheters were used to assess intracavitary pressure, and a flat balloon was used to assess intrapericardial pressure. Right ventricular infarction reduced cardiac output by 23% and stroke volume by 30%. End-diastolic segment length and transmural pressure of the left ventricle decreased. Volume loading restored cardiac output to baseline values and was mediated by a significant increase in end-diastolic length in the noninfarct territory. This was achieved by increasing right ventricular end-diastolic pressure from 9 +/- 2 to 16 +/- 3 mm Hg (p less than 0.01). Partial opening of the pericardium mediated significant increases in both end-diastolic segment lengths of the left ventricle and the noninfarct territory. Left ventricular end-diastolic pressure decreased slightly by 3 mm Hg (p = NS). Complete opening of the pericardium increased cardiac output and stroke volume and mediated a significant decrease in right and left ventricular end-diastolic pressures. Left ventricular transmural pressure and end-diastolic segment lengths of the left ventricle and the noninfarct territory increased. Left ventricular diastolic pressure-segment length relations were shifted upward by right ventricular infarction. A partial opening of the pericardium shifted this relation downward in all animals, and complete opening of the pericardium shifted the relation rightward and further downward. CONCLUSIONS: Cardiac output is restored to baseline values by volume loading sufficient to increase the right ventricular diastolic pressure to 16 +/- 3 mm Hg. Evidence of pericardial constraint was observed and appears to be mediated by an atrioventricular interaction in addition to the direct ventricular interaction.

Animals↗
PubMed1991

Disease severity in the coronary care unit.

The impact of analysis of the severity of illness on the in-hospital mortality was reviewed retrospectively on a cohort of patients admitted to a coronary care unit. Three hundred and eighty-six patients were admitted during the study period, with diagnoses including myocardial infarction (49 percent), unstable angina (23 percent), arrhythmias (11 percent), congestive heart failure (5 percent), and nondiagnostic chest pain (5 percent). Total in-hospital mortality was 13 percent. Severity of illness was measured using the acute physiology and chronic health evaluation (APACHE 2) score. Mortality was found to be influenced by admitting diagnosis (p = 0.01), source of referral (p = 0.03), and APACHE 2 score (nonsurvivors, 16.5 +/- 10.1; survivors, 8.5 +/- 4.8; p less than 0.001). The receiver operating characteristic (ROC) curve for the APACHE 2 confirmed it as a predictor of mortality, with an area under the curve (+/- SE) of 0.75 +/- 0.04 (95 percent confidence limits, 0.67 to 0.83). Logistic regression analysis showed the APACHE 2 score and the diagnosis on admission to be significant multivariate predictors of mortality, and a series of diagnosis-specific coefficients are presented. We conclude that the APACHE 2 score is a useful tool for the overall assessment and management of the CCU, as it is in the multidisciplinary medical-surgical intensive care unit.

Coronary Care Units↗
PubMed1991

Right ventricular diastolic function after experimental right ventricular infarction: effects independent of the pericardium.

To determine if an isolated right ventricular wall infarct (RVI) alters right ventricular diastolic function (RVDF), 6 mongrel dogs were studied before and after a right ventricular wall infarct was produced by ligating the right coronary artery and embolizing the distal right coronary artery with mercury. Right ventricular diastolic function was assessed by prior instrumentation of the animals with an RV Millar catheter and segment length crystals attached to the infarct (I) and non-infarct (NI) territory of the right ventricle. The time constant of RV isovolumic relaxation (Tau) was assessed by fitting right ventricular pressure decline after minimum dp/dt to the equation 1nP = At + B, where A represents the slope of the relationship, a negative number, tau = -1/A. The right ventricular diastolic pressure segment length relationship (RVD PSR) was analyzed using a multiple linear regression model whereby the independent effects of heart rate, segment length, and right ventricular wall infarct could be assessed. Right ventricular wall infarct reduced stroke volume to 63% of baseline values largely by increases in RV-I end-systolic segment length. Tau was significantly prolonged. However, there was no significant upward shift in RVDPSR in any animal. These data suggest that in this model RV diastolic relaxation is impaired. However, the degree of this impairment is not significant enough to shift the right ventricular diastolic pressure segment length relationship, as long as the pericardium remains open.

Animals↗
PubMed1990

Role of prostaglandin E1 in reducing pulmonary vascular resistance in an experimental model of acute lung injury.

To determine the role and efficacy of prostaglandin E1 (PGE1) on the cardiopulmonary derangements induced by glass bead embolism, two studies were performed. In the first study, a dose response of PGE1 was tested in six animals that were first embolized with sufficient glass beads to double the pulmonary artery pressure (PAP). This study demonstrated that PGE1 reduced PAP and cardiac output by a preload-mediated mechanism, as evidenced by a reduction in the right ventricular (RV) end-diastolic segment length, at doses of 15 and 30 ng/kg.min. The second study was performed in two groups of animals, the control group (n = 6), and the treated group (n = 6), which were given PGE1 at 15 ng/kg.min after the PAP had been doubled by glass bead embolism. RV preload was kept constant. This study demonstrated that there was no difference in pulmonary vascular resistance between either the treated group or the control group. There were no other significant differences between the two groups. The results of both of these studies suggest that there is little afterload reducing effect of PGE1 in this model and at these dose ranges. Part of the mechanism of PGE1 that improves pulmonary edema and gas exchange may be the reduction of filtration surface area and hydrostatic pressures in the lungs.

Animals↗