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Biomedical subjects

J T Flaherty

Publications and source records attributed to J T Flaherty.

At least 109 records · Page 6Linked to original sources
PubMed1978

Effects of procaine-induced cardioplegia on myocardial ischemia, myocardial edema, and postarrest ventricular function. A comparison with potassium-induced cardioplegia and hypothermia.

The extent of myocardial protection afforded by a procaine cardioplegic solution during cardiac ischemia has been evaluated and compared with the protection seen using a potassium cardioplegic solution. An isolated cat heart model was employed, and ventricular function parameters, intramyocardial gas tensions, and postischemic myocardial edema were measured and compared following 60 minutes of induced ischemia at 37 degrees C. and 27 degrees C. There was no significant improvement in recovery of postarrest ventricular function when procaine cardioplegia was used during normothermic ischemia. When used at 27 degrees C., however, both cardioplegic solutions were associated with significantly better recovery of postarrest ventricular function, although there was less myocardial edema formation in the potassium-treated hearts. Results of this study indicate that procaine-induced cardioplegia provides myocardial protection during anoxic cardiac arrest which is additive to that afforded by hypothermia alone. In addition, procaine cardioplegia results in postarrest functional recovery which is similar to that seen with potassium cardioplegia.

Animals↗
PubMed1977

Functional significance of coronary arterial stenoses assessed by regional changes in intramyocardial S-T segment voltage and myocardial gas tensions with atrial pacing.

Myocardial carbon dioxide tension and intramyocardial S-T segment voltage have previously been shown to provide useful quantitative indexes of the severity of regional myocardial ischemia. This study was designed to determine if (1) changes in intramyocardial S-T segment voltage and myocardial gas tensions, with the addition of atrial pacing, could be used to assess the functional significance of a coronary stenosis, and (2) if changes in S-T voltage recorded in intramyocardial electrodes proved a more sensitive indicator of ischemia than changes recorded in epicardial electrodes. In 12 open chest dogs, a variable constrictor and an electromagnetic flow probe were placed on the proximal left circumflex coronary artery. Myocardial carbon dioxide and oxygen tensions were recorded with mass spectrometry and unipolar intramyocardial S-T segment voltage with multicontact plunge electrodes. Intramyocardial S-T voltage and myocardial carbon dioxide tension showed parallel increases with atrial pacing in the presence of subcritical, critical and supercritical coronary stenoses. In the presence of a critical stenosis, S-T segment changes recorded in deepr myocardial layers were of greater magnitude than those recorded near the epicardial surface. These findings suggest that the severity of myocardial ischemia can be assessed by measuring intramyocardial S-T voltage or myocardial gas tensions at resting and paced heart rates. They also suggest that intramyocardial S-T voltage is a more sensitive indicator of the severity of pacing-induced myocardial ischemia than epicardial S-T changes. Application of this technique to patients undergoing coronary revascularization could allow intraoperative determination of the functional significance of questionable angiographic lesions and a more rational approach to the assignment of priorities to individual arteries when multiple bypasses are being considered.

Animals↗
PubMed1977

Effects of atrial pacing on regional myocardial gas tensions with critical coronary stenosis.

Changes in myocardial carbon dioxide (PmCO2) and oxygen tension (PmO2) measured by mass spectrometry have been shown to reflect quantitatively progressive degrees of regional myocardial ischemia associated with stepwise reduction in coronary blood flow. The present study utilized mass spectrometry to assess the severity of regional myocardial ischemia developing during atrial pacing in the presence of a flow-limiting proximal critical coronary artend subendocardial layers was measured by the radioactive microsphere technique. Application of a "critical stenosis" resulted in a 6-mmHg decrease in PmO2 and a 17-mmHg increase in PmCO2 in the region of the myocardium supplied by the stenosed vessel. The addition of atrial pacing resulted in a 3-mmHg further decrease in Pmo2 and a 40-mmHg further increase in PmCO2. In the region of myocardium supplied by the critically stenosed vessel MBF increased in the subepicardial layer, but decreased or remained unchanged in the subendocardial layer. The failure of myocardial blood flow to increase in deeper myocardial layers in response to the increased myocardial oxygen demand of atrial pacing would provide a mechanism for the development of subendocardial ischemia in the presence of a critical coronary stenosis.

Animals↗
PubMed1977

Myocardial ischemia during cardiopulmonary bypass. The hazards of ventricular fibrillation in the presence of a critical coronary stenosis.

The effect of a critical coronary artery stenosis on myocardial blood flow and metabolism in the fibrillating heart was assessed by placing 10 dogs on cardiopulmonary bypass, venting the ventricle, inducing ventricular fibrillation, and applying critical stenosis to the left anterior descending coronary artery (LAD). Endocardial and epicardial blood flows were measured by the radioactive microsphere technique prior to the application of the stenosis and after one hour and 2 hours of fibrillation. Intramyocardial oxygen tension (PO2) and carbon dioxide tension (PCO2) were continuously monitored in the LAD-supplied myocardium by a mass spectrometer probe inserted at midmyocardial depth. Selective arterial-coronary venous lactate differences were determined at control, one hour, and 2 hours. At the end of the 2 hour period, vital dye injection defined the distribution of the LAD. Endocardial flow to the myocardium of the stenosed LAD was reduced by 50 per cent after one hour and by 70 per cent after 2 hours (p less than 0.05). Epicardial flow fell 40 per cent after one hour and 50 per cent after 2 hours (p less than 0.05). Endocardial and epicardial flow in the distribution of the unstenosed circumflex coronary artery remained unchanged. Changes in myocardial PO2 and PCO2 in the LAD-supplied myocardium indicated the development of severe ischemia in all 10 dogs and suggested myocardial infarction in 5. There was a conversion from lactate extraction to lactate production during the 2 hour period of ventricular fibrillation. From this study, it is concluded that the myocardium distal to a critical stenosis suffers a progressive reduction in flow during ventricular fibrillation which does not occur in regions supplied by unstenosed coronary arteries. Thus prolonged fibrillation in the presence of a flow-limiting coronary stenosis may play a role in the pathogenesis of myocardial infarction during coronary bypass surgery.

Animals↗
PubMed1977

Regional ischemia distal to a critical coronary stenosis during prolonged fibrillation--improvement with pulsatile perfusion.

In a previous study from this laboratory, regional myocardial ischemia developed distal to a critical coronary stenosis in the fibrillating heart on cardiopulmonary bypass when myocardial perfusion was non-pulsatile. To assess the effect of pulsatile perfusion on the development of the fibrillation-induced ischemia, 10 dogs were placed on total cardiopulmonary bypass with the heart in the vented fibrillating state. A critical stenosis was applied to the left anterior descending artery (LAD). Pulsatile perfusion with a pulse pressure of 35 mm Hg and a pulse rate of 100/min was produced by a new method developed in this laboratory. During the 2 hours of bypass, ischemia in the LAD-supplied myocardium was assessed by changes in intramyocardial oxygen (PmO2) and carbon dioxide (PmCO2) tensions and by regional arterial-coronary venous lactate difference. With linear perfusion, regional ischemia in the LAD myocardium had been evidenced by a low PmO2 (8 +/- 3 mm Hg), a high PmCO2 (170 +/- 25 mm Hg) and regional lactate production (9.2 +/- 4.2 mg/100 ml). In contrast with pulsatile perfusion intramyocardial gas tensions remained stable during the 2 hours on bypass (PmO2 = 21 +/- 3 mm Hg, PmCO2 = 65 +/- 5 mm Hg, P less than 0.05 vs linear flow study) and lactate consumption was demonstrated (+17.7 +/- 2.9 mg/100 ml, P less than 0.001 vs linear flow group). With linear perfusion, myocardial blood flow to the LAD area had decreased 56 +/- 8% in the subendocardial layer and 46 +/- 7% in the subepicardial layer. In the dogs receiving pulsatile flow during bypass, regional LAD blood flow remained unchanged over the 2-hour bypass period and was significantly higher than the flow with linear flow (P less than 0.05). These data indicate that fibrillation-induced regional myocardial ischemia distal to a critical stenosis can be prevented by maintaining pulsatile perfusion during cardiopulmonary bypass.

Animals↗
PubMed1976

Effects of intravenous nitroglycerin on left ventricular function and ST segment changes in acute myocardial infarction.

It has been shown previously that 30-minute infusions of intravenous nitroglycerin in patients with acute myocardial infarction are able to lower left ventricular filling pressure and improve left ventricular function while lowering mean arterial pressure by only 7 mmHg (0.9 kPa). A decrease in sigmaST in praecordial ST segment mapping studies during nitroglycerin infusion in patients with anterior infarction suggested a decrease in the extent of myocardial ischaemia. In the present study, 30 patients with acute myocardial infarction received 1- to 3-hour infusions of intravenous nitroglycerin at infusion rates sufficient to lower mean arterial pressure by an average of 22 mmHg (2.9 kPa). An improvement in ventricular function was noted in that subgroup of patients with the msot severe left ventricular dysfunction. All patients with anterior myocardial infarction underwent serial ST segment mapping and, irrespective of the presence or absence of left ventricular failure, showed a decrease in sigmaST during nitroglycerin infusion (P less than 0.005). These findings suggest that infusion of nitroglycerin improves left ventricular function and/or alters left ventricular compliance in patients with left ventricular failure complicating myocardial infarction and furthermore decreases sigmaST in all patients, irrespective of the presence or absence of left ventricular failure, suggesting that the extent of myocardial ischaemia is decreased.

Acute Disease↗
PubMed1976

A new method of producing pulsatile flow during cardiopulmonary bypass using a standard roller pump.

A new method for producing pulsatile flow during cardiopulmonary bypass is described. The method requires only the addition of a dilated segment in the tubing which passes beneath the arc of a standard roller pump. Preliminary studies demonstrate that pulsatile flow and pressure with physiologic contours can be produced by this "bubble tube" system. Furthermore, the new tubing causes less hemolysis than standard pump tubing.

Animals↗
PubMed1975

Reversal by phenylephrine of the beneficial effects of intravenous nitroglycerin in patients with acute myocardial infarction.

Nitroglycerin has been shown to reduce ST-segment elevation during acute myocardial infarction, an effect potentiated in the dog by agents that reverse nitroglycerin-induced hypotension. Our study was designed to determine the effects of combined nitroglycerin and phenylephrine therapy. Ten patients with acute transmural myocardial infarctions received intravenous nitroglycerin, sufficient to reduce mean arterial pressure from 107 +/- 6 to 85 +/- 6 mm Hg (P less than 0.001), for 60 minutes. Left ventricular filling pressure decreased from 19 +/- 2 to 11 +/- 2 mm Hg (P less than 0.001). SigmaST, the sum of ST-segment elevations in 16 precordial leads, decreased (P less than 0.02) with intravenous nitroglycerin. Subsequent addition of phenylephrine infusion, sufficient to re-elevate mean arterial pressure to 106 +/- 4 mm Hg (P less than 0.001) for 30 minutes, increased left ventricular filling pressure to 17 +/- 2 mm Hg (P less than 0.05) and also significantly increased sigmaST (P less than 0.05). Our results suggest that addition of phenylephrine to nitroglycerin is not beneficial in the treatment of patients with acute myocardial infarction.

Acute Disease↗
PubMed1975

Atypical posterior leaflet motion in echocardiogram in mitral stenosis.

The echocardiographic diagnosis of mitral stenosis is based on the finding of a decreased early diastolic slope of the anterior mitral leaflet. This finding is also seen in other conditions in which the rate of left ventricular filling is reduced by decreased compliance of the ventricular myocardium rather than by mitral valve obstruction. Patients with "true" mitral stenosis have been differentiated from those with decreased ventricular compliance resulting in "false" mitral stenosis by the direction of movement of the posterior mitral valve leaflet. This report describes a patient with mitral stenosis proved at cardiac catheterization whose echocardiogram showed posterior motion of thickened posterior mitral leaflet during diastole, a finding previously considered to exclude organic mitral stenosis. This false negative echocardiographic finding in proved mitral stenosis has not previously been reported.

Adolescent↗
PubMed1975

Intravenous nitroglycerin in acute myocardial infarction.

Vasodilator therapy has been shown to improve ventricular function in patients with left ventricular failure complicating acute myocardial infarction. Sublingual nitroglycerin also improves ventricular function in these patients but its effects are transient and variable. Infusion of intravenous nitroglycerin in 12 patients with acute infarction resulted in a decrease in left ventricular filling pressure from a mean of 22 plus or minus 2 mm Hg to 12 plus or minus 1 mm Hg (P less than 0.001) associated with a 7 mm Hg decrease in mean arterial pressure (P less than 0.05). Since stroke work index did not change significantly, this represents and improvement in ventricular performance and/or an alteration in ventricular compliance. All six patients in whom serial precordial mapping studies were performed showed a decrease in sigma ST (P less than 0.001). These findings suggest that intravenous nitroglycerin improved left ventricular function and decreased the extent of myocardial ischemia. Longer infusion may act to preserve borderline ischemic myocardium and thus limit infarct size.

Administration, Oral↗
PubMed1975

Changes in intramyocardial ST segment voltage and gas tensions with regional myocardial ischemia in the dog.

This study was designed to evaluate the sensitivity of changes in myocardial carbon dioxide and oxygen tensions as indicators of regional myocardial ischemia and also to determine to what extent these changes can be related to changes in intramyocardial ST segment voltage. Changes in ST segment voltage recorded in unipolar epicardial electrodes proved to be a less-sensitive indicator of underlying myocardial ischemia than were changes in ST segment voltage recorded in unipolar intramyocardial electrodes. In 9 dogs, regional ischemia was produced by placing a variable constrictor on the left circumflex coronary artery; circumflex flow was monitored. Myocardial carbon dioxide and oxygen tensions were measured using a mass spectrometer. Unipolar electrograms were recorded using a multicontact plunge electrode. With progressive degrees of proximal stenosis, ranging from a critical stenosis, which is associated with a decrease in mean flow of less than 15%, to a severe stenosis associated with and 80% decrease, ST voltage increased 21 mv and carbon dioxide tension increased 84 mm Hg, but oxygen tension decreased only 7 mm Hg. The study suggests that increases in intramyocardial ST segment voltage, an index of myocardial ischemia, are associated with parallel increases in myocardial carbon dioxide tension, each providing a more sensitive quantitative correlate of regional myocardial ischemia than do decreases in oxygen tension. The local accumulation of carbon dioxide may be an important pathophysiological mechanism in myocardial ischemia.

Animals↗
PubMed1975

Mass spectrometry for the measurement of intramyocardial gas tensions: methodology and application to the study of myocardial ischemia.

The methodology for use of the mass spectrometer for the measurement of intramyocardial gas tensions in the canine preparation is described. Baseling studies were carried out initially in 36 animals, and control levels for myocardial oxygen tension and myocardial carbon dioxide tension were 19 mm Hg (S.D. 6 mm Hg) and 43 mm Hg (S.D. 10 mm Hg), respectively. Myocardial oxygen tension was not altered significantly by varying the arterial oxygen tension between 65 and 300 mm Hg. However, myocardial carbon dioxide tension increased linearly with increased arterial carbon dioxide tension. In 15 dogs placed on total cardiopulmonary bypass, a perfusion pressure 40-60 mm lower than the control mean arterial pressure resulted in myocardial ischemia with a decrease in myocardial oxygen tension and an increase in myocardial carbon dioxide tension. A subsequent increase in perfusion pressure to control levels resulted in resolution of ischemia and return of myocardial oxygen and carbon dioxide tensions to their control level. In another series of open-chest dogs on cardiopulmonary bypass, a proximal constriction applied to the left coronary circumflex artery resulted in a marked decrease in myocardial oxygen tensions and a marked increase in myocardial carbon dioxide tensions in the region supplied by the constricted vessel. In yet another series of open-chest dogs, it was found that incremental decreases in coronary flow established by constriction of the circumflex artery resulted in an exponential increase in both myocardial carbon dioxide tensions and ST-segment elevation as determined by a 25-gauge multi-contact plunge electrode placed in the posterior left ventricular wall. It appears that mass spectrometry techniques for evaluating myocardial ischemia have several advantages over myocardial biopsy techniques for assay of ATP and lactate, and also over the technique of coronary sinus lactate determination.

Animals↗