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Biomedical subjects

C W Hamm

Publications and source records attributed to C W Hamm.

At least 19 recordsLinked to original sources

The prognostic value of serum troponin T in unstable angina.

BACKGROUND: Cardiac troponin T is a regulatory contractile protein not normally found in blood. Its detection in the circulation has been shown to be a sensitive and specific marker for myocardial cell damage. We used a newly developed enzyme immunoassay for troponin T to determine whether its presence in the serum of patients with unstable angina was a prognostic indicator. METHODS: We screened 109 patients with unstable angina (25 with accelerated or subacute angina and 84 with acute angina at rest) for serum creatine kinase activity, creatine kinase isoenzyme MB activity, and troponin T every eight hours for two days after admission to the hospital. The outcomes of interest during the hospitalization were death and myocardial infarction. RESULTS: Troponin T was detected (range, 0.20 to 3.64 micrograms per liter; mean, 0.78; median, 0.50) in the serum of 33 of the 84 patients (39 percent) with acute angina at rest. Only three of these patients had elevated creatine kinase MB activity (two were positive for troponin T, and one was negative). Of the 33 patients who were positive for troponin T, 10 (30 percent) had myocardial infarction (3 after coronary-artery bypass surgery), and 5 of these died during hospitalization. In contrast, only 1 of the 51 patients with angina at rest who were negative for troponin T had an acute myocardial infarction (P less than 0.001), and this patient died (P = 0.03). Thus, 10 of the 11 patients with myocardial infarctions had detectable levels of troponin T; only 1 had elevated creatine kinase MB activity. Troponin T was not detected in any of the 25 patients with accelerated or subacute angina, and none of these patients died. CONCLUSIONS: Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial-cell injury than serum creatine kinase MB activity, and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina.

Aged

Recovery of myocardial function in the hibernating heart.

Impaired contractile performance at rest is not necessarily due to irreversible tissue damage but may relate to the "hibernating" myocardium. Hibernating myocardium has been defined as potentially reversible, chronic contractile dysfunction during prolonged, painless ischemia. The extent and time course of functional recovery after restoration of flow is of major importance for clinical decision making. The existence of hibernating myocardium was first documented in patients following bypass surgery. Angiographic studies in patients undergoing coronary angioplasty revealed immediate recovery of global and regional systolic, as well as diastolic, function after revascularization. Subgroup analysis showed an improvement in patients without previous myocardial infarctions and in those with non-Q-wave infarctions, but a benefit was not consistently seen in patients with transmural infarctions. A further improvement of systolic function after 15 weeks suggests a biphasic course of recovery. Prospective studies must clarify whether the potential for improvement in function constitutes an indication for revascularization independent of clinical symptoms.

Angioplasty, Balloon, Coronary

Residual platelet function under acetylsalicylic acid and the risk of restenosis after coronary angioplasty.

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) was shown not to be preventable by antiplatelet therapy; residual platelet function under treatment with platelet inhibitors could be one cause of this. Therefore, in a prospective investigation, residual platelet function was assessed in 98 patients treated with acetylsalicylic acid (ASA) on three occasions during the first 3 months after successful PTCA. Control cardiac catheterization was obtained in 75 of these patients (77%) with 82 dilated stenoses 173 +/- 117 days after PTCA. Restenosis, defined as diameter stenosis greater than or equal to 50% at control angiography, occurred in 41% of the dilated vessels, and 43% of patients experienced restenosis in at least one vessel. The in vitro platelet aggregatory response to either ADP (0.5, 1, and 10 microM) or collagen (1 and 5 mg/L) as aggregating agents did not differ between patients with and without restenosis. In addition, neither the collagen-stimulated in vitro synthesis of thromboxane nor the basal or prostaglandin E1-stimulated concentrations of cyclic AMP in platelet-rich plasma (PRP) was different in the two groups. There was no significant correlation between any of the parameters of platelet function assessed and the change in coronary luminal diameter observed between immediately after PTCA and control coronary angiography. The mean dose of ASA ingested during follow-up was also not a determinant of the occurrence of restenosis. Thus, residual platelet function under treatment with ASA as measured in vitro in this study, did not influence the occurrence of restenosis after successful PTCA.

Angioplasty, Balloon, Coronary

[Peripheral embolism of hemostasis collagen (VasoSeal)].

VasoSeal is a purified bovine, absorbable collagen plug currently successfully used to close the femoral arterial puncture site after cardiac catheterization under full anticoagulation. Up to now there has been no experience with potential complications. We observed acute ischemia in the right lower leg of 2/100 patients 36 resp. 24 h after successful closure of the puncture site with VasoSeal. Angiography confirmed acute occlusion of the distal A. poplitea dextra. A 25-mm resp. 50-mm long cylindrical foreign body embolus was removed with a Fogarty-catheter by retrograde indirect embolectomy. Histopathology confirmed a fresh collagen clot with appositional thrombosis.

Aged

[Cardiovascular risk factors and restenosis after PTCA].

We prospectively investigated the influence of the cardiovascular risk factors hypercholesterolemia, smoking, diabetes mellitus, and arterial hypertension on the occurrence and extent of restenosis after successful coronary dilatation (PTCA). Of the 103 patients included in the study, control coronary angiography was obtained in 75 (73%) after 173 +/- 117 days. The restenosis rate (82 stenoses), defined as greater than or equal to 50% loss of initial gain in percent diameter stenosis, was 37%. Older age, male gender, and a history of diabetes mellitus were associated with a significantly increased mean extent of restenosis (p less than 0.05). In patients with hypertension, the initial success of dilatation was less than in controls without hypertension (p less than 0.05), and restenosis tended to be enhanced (p = 0.06). The risk of restenosis was unaffected by smoking and the presence of hypercholesterolemia. In spite of the mostly insignificant influence of single cardiovascular risk factors, the extent of restenosis clearly increased with the number of risk factors.

Aged

Delayed coronary occlusion following primary successful angioplasty: management and outcome.

The treatment of delayed coronary occlusion after primary successful percutaneous transluminal coronary angioplasty (PTCA) is more difficult because surgical standby is often not available. The purpose of this study was to assess the therapeutic approaches and outcome of patients with delayed coronary occlusion from 30 to 180 minutes after successful PTCA. A delayed occlusion occurred in 18 (0.9%) (61 +/- 11 years; male n = 14, female n = 4) out of 2065 consecutive patients after PTCA. In 11 patients the dilated stenoses were located in the left descending artery, while seven patients had the stenosis in the right coronary artery. Twelve patients had unstable or postinfarction angina. The time interval between completion of PTCA and the onset of chest pain was 64 +/- 39 minutes. Immediate i.v. nitroglycerin resulted in no relief of the symptoms in any patient. One patient was operated upon at once, and one was given i.v. thrombolysis resulting in pain relief and reversal of ECG changes. The remaining 16 patients returned initially to the catheterization laboratory, where the occluded vessels were opened by mechanical recanalization. Three of them remained in stable condition. Due to impending reocclusion surgery was necessary in four patients and thrombolysis was performed in nine. After thrombolysis the vessel remained open in four patients. The other five needed bypass surgery on the day of PTCA. Myocardial infarction developed in nine patients (maximal CK 673 +/- 488 units/l). In conclusion, delayed occlusion after successful PTCA is a rare complication occurring primarily in patients with unstable angina. Mechanical recanalization opened the occluded vessel in most patients, and myocardial infarction was prevented in 50%.

Adult

[Improvement of chronic regionally impaired myocardial function immediately after coronary angioplasty].

UNLABELLED: The effect of PTCA on chronically impaired, regional wall motion was studied in 40 patients with stable angina and stenoses in the left anterior descending artery. Left-ventricular angiograms were obtained before, 15 min after PTCA and, additionally, in eight patients 15 +/- 5 weeks after PTCA. Left-ventricular ejection fraction and regional myocardial function were assessed by the centerline method. Patients with no (n = 18) or non-Q-wave (n = 12) infarction were compared to patients with Q-wave infarction (n = 10). After PTCA, ejection fraction increased from 54 +/- 8% to 59 +/- 8% (p less than 0.05) and regional function improved significantly (maximal standard deviation before PTCA: 2.8 +/- 0.8; after PTCA: 1.9 +/- 0.9- segments below the first standard deviation before PTCA: 31 +/- 16; after PTCA: 19 +/- 17). The improvements were found in patients with no or non-Q-wave infarction. The benefit on regional function was unchanged at follow-up. CONCLUSIONS: PTCA reduced chronic regional myocardial dysfunction in 78% of the patients with stable angina within 15 min. Reversible myocardial dysfunction is most likely related to hibernating myocardium.

Aged

Recanalization of chronic, totally occluded coronary arteries by new angioplasty systems.

The benefit and safety of new angioplasty equipment as compared with the conventional guidewire approach was evaluated in 154 consecutive patients. with chronic, totally occluded coronary arteries. The protocol followed a stepwise design: first, conventional guidewires and low-profile balloons were used, followed by "balloon-on-the-wire" systems (Probe, Ace) or by a shaft-enforced, tip-deflecting catheter (Omniflex). In 97 patients with occlusions of 2 to 12 weeks' duration, recanalization was achieved in 51 patients (53%) with the conventional approach and in 29 patients with the new devices (balloon-on-the-wire [n = 5], Omniflex [n = 24]), thereby raising the success rate to 82%. In 57 occlusions of greater than 12 weeks' duration, the recanalization attempt was successful in 58%, mediated in 16 patients (28%) by the Omniflex catheter and in 5 patients by balloon-on-the-wire systems. There were no life-threatening complications and only 1 (0.6%) emergency bypass operation was necessary. New angioplasty devices are therefore of considerable value in the attempt to improve the results of coronary angioplasty in chronic total occlusions.

Angioplasty, Balloon, Coronary

A prospective study of the diagnostic value of urinary thromboxane in patients presenting with acute chest pain.

In chance single-case observations thromboxane excretion has been reported to increase several days prior to myocardial infarction. To test its frequency and potential diagnostic value we prospectively measured thromboxane excretion in 166 consecutive patients who had presented to the emergency unit with acute chest pain indicative of ischaemia. Thromboxane excretion at presentation was increased, sometimes dramatically, in 17 of 33 (52%) patients with unstable angina, in 42 of 73 (57%) patients with definite myocardial infarction, but in only two of 14 (14%) patients with stable angina. Nineteen of 29 patients undergoing early angiography had detectable intracoronary thrombi, and these patients excreted significantly more thromboxane than patients without thrombi. Ongoing platelet activation may be detected by increased thromboxane excretion in more than 50% of the patients presenting with unstable angina and myocardial infarction, particularly in those with intracoronary thrombi, but it is not a general phenomenon that can be used in diagnosis.

Aged

[Radiologic methods in cases of coronary heart disease: diagnostic requirements from the cardiology point of view].

Radiological and especially scintigraphic methods are important tools in diagnosis finding, diagnosis evaluation, risk stratification and therapy control in patients with coronary artery disease. The major task is to document or exclude myocardial perfusion defects. Within this framework, thallium scintigraphy and radionuclide ventriculography occupy a definite place for non-invasive evaluation. The decision for revascularisation (bypass surgery, angioplasty) and the evaluation of the risk frequently depends on the results of the scintigraphic methods. Conventional radiological techniques and computer tomography are helpful in differential diagnosis of acute chest pain syndromes.

Coronary Disease

Critical role of dose in protection by propranolol against ventricular fibrillation in a pig model of acute myocardial ischemia.

We hypothesized that the antiarrhythmic efficacy of propranolol during acute myocardial ischemia could be dose related. Propranolol was administered in two equally divided doses 30 min before and 10 min after ligation of the anterior descending coronary artery (CAL) in anesthetized open-chest pigs. Only the lowest dose of propranolol, i.e., 0.1 mg/kg intravenously (i.v.) (plasma level 22 +/- 2 ng/ml) decreased the incidence of ventricular fibrillation (VF), i.e. 3 of 12 versus 16 of 20 in control group (p less than 0.01). VF incidence with propranolol 0.5 or 3 mg/kg was 4 of 6 and 8 of 9, respectively (both NS vs. control group). Propranolol 0.1 mg/kg did not change left ventricular (LV) blood flow. Propranolol 3 mg/kg reduced blood flow in the peripheral ischemic myocardium to 13.2 +/- 1.2 versus 19.2 +/- 1.4 ml/100 g/min in control group (p less than 0.01), and in the midischemic zone to 4.4 +/- 0.5 versus 7.0 +/- 0.9 ml/100 g/min in control group (p less than 0.001). Propranolol 0.1 mg/kg prevented a disparity of levels of cyclic AMP from arising between ischemic and non-ischemic myocardium, whereas propranolol 3.0 mg/kg did not. Furthermore, LV mechanical function was suppressed by propranolol 3 mg/kg. Only the lowest dose of propranolol (i.e., 0.1 mg/kg) decreased the incidence of VF in this model.

Adenosine Triphosphate

[Thrombocyte function in unstable angina pectoris].

In a prospective study, platelet aggregation in platelet-rich plasma after ADP stimulation (0.5, 1.0 and 10 mumol/l) and collagen (1 and 5 micrograms/ml) was measured in 36 patients with coronary heart disease, 18 with angina at rest during the eight hours preceding the time of blood sampling, and 18 patients with stable, exercise-dependent angina, matched for age and sex. In addition, c-AMP was determined, before and (as a measure of platelet adenylate cyclase activity) after stimulation of this enzyme by prostaglandin E1 (10 mumol/l for 30 sec). There were no differences between all the tested ADP and collagen concentrations with regard to platelet aggregation. c-AMP levels were also similar. Thus, in patients with unstable angina there was no evidence for generalized hyperaggregation of platelets in comparison with control subjects who had stable exercise-dependent angina.

Adenosine Diphosphate

Unstable angina: current concepts of medical management.

Unstable angina describes a clinical syndrome bridging the gap between stable angina and acute myocardial infarction. By definition, patients with angina of new onset, of a crescendo pattern, and with angina at rest are included in this high-risk group. The underlying pathogenetic mechanisms are complex and include initial atherosclerotic plaque rupture, release of vasoactive substances, and intracoronary thrombus formation. The currently established medical approach of the acute phase consists of heparin for anticoagulation and nitrates combined with beta-blockers for the relief of pain. Calcium antagonists are indicated, if anginal symptoms persist. The effect of thrombolytic therapy is still under investigation. Angina refractory to medical treatment and angina at rest are associated with a particularly unfavorable prognosis and prompt early catheterization. The long-term prognosis of the patient is markedly improved by chronic platelet inhibitory treatment with aspirin.

Angina, Unstable

Quantitation of coronary venous adenosine in patients: limitations evaluated by radioimmunoassay.

Experimental studies have shown that adenosine is rapidly released in response to myocardial ischaemia. To evaluate whether coronary venous adenosine release is a metabolic characteristic of myocardial ischaemia in patients, adenosine concentrations were measured by a highly sensitive and specific radioimmunoassay. In three patients with normal coronary arteries and in seven with obstructive coronary artery disease coronary venous adenosine content was measured at rest and during atrial pacing. When whole blood or plasma were extracted immediately with perchloric acid the adenosine content was found to be lower than that previously reported. Recovery studies showed that the importance of time and temperature at low adenosine concentrations had been underestimated in preceding studies. In patients with coronary artery disease coronary venous adenosine concentration increased from 106.3(48.8) nmol.litre-1 to 114.9(57.0) nmol.litre-1 (NS) during pacing and was 130.4(63.3) nmol.litre-1 (NS) 2 min after pacing. Even in the presence of lactate production enhanced adenosine release was not consistently evidenced. Furthermore, venous adenosine content did not increase in five patients undergoing coronary artery occlusion during angioplasty of the left anterior descending coronary artery. The extremely short half life of coronary venous adenosine appears to preclude its use as an index of myocardial ischaemia in patients.

Adenosine