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Biomedical subjects

D Durrer

Publications and source records attributed to D Durrer.

At least 73 records · Page 4Linked to original sources

Prevalence of right ventricular involvement in inferior wall infarction assessed with myocardial imaging with thallium-201 and technetium-99m pyrophosphate.

To assess the prevalence and clinical relevance of right ventricular involvement in acute inferior wall infarction, 78 consecutive patients with the latter condition were studied with thallium-201 and technethium-99m pyrophosphate myocardial imaging. Right ventricular involvement was determined from superimposition of the 45 degree left anterior oblique thallium-201 and technetium-99m pyrophosphate images. All 78 patients shoed thallium-201 defects. Sixty-four patients had positive pyrophosphate scans, and 24 of these (37.5 percent) showed right ventricular involvement. None of the patients with right ventricular involvement in this consecutive series showed the classic signs of severe right ventricular failure, although subclinicalright ventricular dysfunction may have been present. There was no significant difference in the incidence of cardiogenic shock between the groups with and without right ventricular involvement. It is concluded that right ventricular involvement in acute inferior wall infarction is relatively frequent but not necessarily associated with severe right-sided pump failure. In patients with acute inferior wall infarction and severe pump failure, dual imaging provides a simple nonivasive method of identifying the subgroup of patients with right ventricular involvement who may benefit from volume loading.

Adult↗

Efficacy of lidocaine in preventing primary ventricular fibrillation within 1 hour after a 300 mg intramuscular injection. A double-blind, randomized study of 300 hospitalized patients with acute myocardial infarction.

The effectiveness of intramuscular lidocaine in preventing in-hospital primary ventricular fibrillation within 1 hour after injection of the drug in patients with acute myocardial infarction was assessed in a double-blind randomized study performed in 300 such patients admitted within 6 hours of myocardial infarction. Six of 147 patients treated with 300 mg of intamuscular lidocaine had ventricular fibrillation compared with 4 of 153 control subjects. The lidocaine blood level of the patients who experienced ventricular fibrillation was 1.4 +/- 0.7 microgram/ml (mean +/- standard deviation) at the time of fibrillation, a value not significantly different from that of treated patients who did not experience fibrillation. Lidocaine blood levels in the latter were 1.9 +/- 1.1, 2.1 +/- 1.1, 2.1 +/- 1.1 and 1.7 +/- 0.7 microgram/ml, respectively, 7, 15, 30 and 60 minutes after injection. In this study intramuscular lidocaine was ineffective in preventing ventricular fibrillation, possibly because the given dose, 300 mg, prevented attainment of adequqte blood levels of the drug.

Adult↗

Thallium-201 scintigraphy in unstable angina pectoris.

Thallium-201 scintigraphy was performed during the pain free period in 98 patients with unstable angina. Scintiscans were positive in 39 patients, questionable in 27 patients and normal in 32 patients. Eighty-one patients responded favorably to treatment (group I). Seventeen patients had complicated courses (group II) and despite maximal treatment with propranolol either developed infarction (six patients) or continued to have angina necessitating coronary surgery (11 patients). In group I during the pain free period 26 of 81 patients had positive thallium-201 scans, whereas 20 patients had an abnormal ECG at that time; during angina 18 patients had transient ECG changes. In group II during the pain free period 13 of 17 patients had positive scans, whereas two patients had abnormal ECG at that time; during angina 12 patients showed transient ECG changes. The sensitivity to recognize group II was 76% for thallium-201 scintigraphy, 11% for ECG during the pain free period; 70% for ECG during angina; 94% for the combination of either positive scans or abnormal ECG. Thus, 1) positive thallium-201 scans occur in patients with unstable angina, 2) positive scans can be obtained during the pain free period, 3) thallium-201 scans are more frequently positive in patients with complicated course.

Angina Pectoris↗

The anatomical substrates of wolff-parkinson-white syndrome. A clinicopathologic correlation in seven patients.

Clinicopathological correlations were made on the hearts from seven patients known to have exhibited electrocardiographic evidence of the Wolff-Parkinson-White syndrome. In each case, clinical and pathological investigations were conducted independently, neither group of investigators having knowledge of the other's results. In all seven hearts, the entire atrioventricular junctions were serially sectioned. Accessory atrioventricular connections were predicted in all seven cases following electrocardiographic investigation. Connections were identified histopathologically in four hearts in the predicted site. In another case two connections were identified, one being considered responsible for the pre-excitation. In the sixth case a right lateral connection was anticipated, but only accessory nodo-ventricular fibers were identified following histopathologic studies. In the final case, a posterior septal connection was predicted but the entire septum had fibrosed following previous operation. These findings are discussed in the light of the investigative techniques used, the theories of pre-excitation and the embryogenetic mechanisms producing accessory atrioventricular connections.

Adult↗

Mechanisms of tachyarrhythmias, past and present.

Several hypotheses, developed in the early years of arrhythmology, and frequently used for the explanation of many types of clinical tachyarrhythmias, are often based on experiments on unusual models, unphysiologic interventions, or, in some instances, on erroneously interpreted histologic findings. However, it can be demonstrated that several of these hypotheses are valid. Focal activity, unidirectional block, extremely slow conduction velocity, differences in conduction velocity in closely adjacent regions, reentry of the excitation wave, circulating excitation waves in small or large regions of the heart and other postulated mechanisms as, for example, entrance and exit block, local ventricular fibrillation, appear to be involved in the causative mechanisms of clinical tachyarrhythmias. A multicausal genesis of at least some of these must be considered seriously, particularly those which occur in acute or chronic coronary heart disease. A recent suggestion that the injury current might be involved in the genesis of ventricular tachyarrhythmias in acute myocardial ischemia and infarction is supported by observations on several properties of this current. Progress has been made in recent years but large gaps in our knowledge of mechanisms causing arrhythmias are still present.

Animals↗

The effect of "ischemic" blood on transmembrane potentials of normal porcine ventricular myocardium.

"Ischemic" blood was obtained in pigs from a local coronary vein on release of coronary artery occlusion. The effects of this blood on transmembrane potentials of muscle strips taken from the same heart were compared with control blood. Whereas action potentials remained stable in control blood, ischemic blood collected after more than 15 minutes of coronary occlusion produced shortening of action potential duration, reduction of resting potential, upstroke velocity and amplitude, then postrepolarization refractoriness and finally unresponsiveness. Ischemic blood collected after shorter periods of coronary occlusion produced only mild effects (shortening of action potential and postrepolarization refractoriness). These effects of ischemic blood could not be attributed to increased potassium concentration even in combination with acidosis, hypoxia and hypoglycemia. It appears that during ischemia unidentified factors are released which have potent depressant effects on the excitability of even normal myocardium.

Action Potentials↗

Location and size of acute transmural myocardial infarction estimated from thallium-201 scintiscans. A clinicopathological study.

A clinicopathological study was performed in 23 patients who died from acute transmural myocardial infarction and who had been studied with thallium-201 during the acute phase. Twenty patients died within five days and three later than five days after scintigraphy. The scintigraphic location and the estimated size of infarction in vivo were correlated with postmortem findings. There was good agreement in 91% between scintigraphic and postmortem location of infarction and in 70% between the ECG and postmortem findings. The size of infarction as determined from computer-processed schematic drawings of postmortem slices of the heart correlated well with the size determined from processed schematic drawings of the scintiscans (r = 0.91 for anterior infarction, r = 0.97 for inferior infarction, r = 0.86 for anterior-inferior infarction). It is concluded that thallium-201 scintigraphy provided more precise location of infarction than the ECG and that the size of the scintigraphically abnormal area reflected the extent of necrotic myocardium.

Humans↗

The effect of acute coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart.

Subepicardial transmembrane potentials were recorded from intact pig hearts to observe the changes induced by acute ischemia. Ischemia shortened action potential duration, and decreased its amplitude, upstroke velocity, and resting potential. The cells were unresponsive after 12 to 15 minutes of coronary artery occlusion, yet near normal action potentials could be restored by flushing the occluded artery with saline as late as 40 minutes after occlusion. The unipolar extracellular electrogram reflected unresponsiveness by a monophasic potential. Local refractory periods initially shortened by up to 100 msec. Later, postrepolarization refractoriness occurred and refractory periods lengthened often in excess of basic cycle length, thus resulting in 2:1 responses. The onset of early ventricular arrhythmias often coincided with a period of alternation and 2:1 responses, especially when these got out of phase in different regions. Reperfusion frequently led to ventricular fibrillation, and was associated with marked inhomogeneity in cellular responses. Re-entry within ischemic myocardium was the most likely mechanism for arrhythmias.

Action Potentials↗

Treatment and prevention of primary ventricular fibrillation complicating acute myocardial infarction.

Primary ventricular fibrillation especially occurs during the first hours after acute myocardial infarction and is often not preceded by premonitory ventricular premature beats. In hospital primary ventricular fibrillation can be prevented by an intravenous lidocaine regimen in a rather high dosage. By contrast the effectiveness of intramuscular lidocaine in preventing out-hospital primary ventricular fibrillation is unestablished. If recurrent attacks of primary ventricular fibrillation supervene, intervention with antiarrhythmic therapy and/or cardiac pacing is often unsuccessful. Repeated defibrillation should be carried out under these circumstances. If properly treated primary ventricular fibrillation is associated with a good short and long term prognosis.

Electric Countershock↗