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Biomedical subjects

T Killip

Publications and source records attributed to T Killip.

At least 55 records · Page 3Linked to original sources
PubMed1977

Left ventricular performance and graft patency after coronary artery-saphenous vein bypass surgery: early and late follow-up.

Left ventircular performance and graft patency were studied postoperatively at 2 weeks in 19 patients, and at 9 months in 15 patients. At early follow-up, left ventricular ejection fraction and mean rate of circumferential shortening were unchanged for the group as a whole, but were slightly improved in patients who had had a moderately abnormal preoperative ejection fraction of 0.30 to 0.60. At late follow-up, 10 of 14 patients had occluded at least one graft or the proximal segment of the grafted coronary artery and had an associated decrease in ventricular function. The risk of graft occlusion was greater if the preoperative ejection fraction was decreased; seven of 10 patients with a preoperative EF of less than 0.60 suffered one or more graft occlusions, but only three of 16 patients with a preoperative EF greater than 0.60 had a postoperative graft occlusion (p is less than 0.05). The results suggest that bypass graft surgery is not generally indicated as a measure to improve ventricular function in patients with ischemic heart disease.

Angina Pectoris↗
PubMed1976

Aspirin therapy in angina pectoris: effects on platelet aggregation, exercise tolerance, and electrocardiographic manifestations of ischemia.

If altered platelet function contributes to poorly perfused zones of myocardium in patients with angina pectoris, then specific antiplatelet therapy might improve cardiovascular function and exercise performance. Exercise tolerance on a bicycle ergometer, heart rate-blood pressure product, and ischemic ECG changes at exercise end-point were compared before and during oral aspirin therapy (2.4 Gm. per day for 2 weeks) in 11 normal subjecs and in 11 patients with stable angina pectoris. Platelet aggregation threshold in response to ADP and epinephrine was measured. Untreated patients had increased platelet aggregability when compared to normal subjects...

Adult↗
PubMed1975

Variant angina pectoris.

A patient with variant angina pectoris due to a pedunculated calcific mass extending from the aortic valve and resulting in intermittent obstruction of the left coronary ostia is reported. No atherosclerotic disease was demonstrated by coronary angiography. During attacks, marked ST segment elevation and episodes of tachycardia were associated with a moderate rise in pulmonary artery pressure. Replacement of the calcified aortic valve resulted in total relief of symptomatology.

Angina Pectoris↗
PubMed1975

Noninvasive assessment of clinical response to oral propranolol therapy.

Nineteen patients with severe but stable angina pectoris entered a double blind controlled study to evaluate the effect of orally administered propranolol on exercise tolerance measured with a bicycle ergometer, and left ventricular function measured by echocardiography and systolic time intervals. In the group treated with propranolol the dose was increased from 80 to 320 mg/day. Studies including determination of propranolol blood levels were obtained before treatment and for each dose of propranolol. With propranolol, 80 mg/day, total work performance increased by 128 percent from 765 plus or minus 125 before treatment to 1,792 plus or minus 285 kilopond-meters (mean plus or minus standard error) (P less than 0.01). With 160 mg of propranolol daily, total work performance decreased, but remained higher than at control levels. In the group given propranolol, left ventricular function decreased progressively with increasing doses of the drug. As measured from the echocardiogram, maximal endocardial posterior wall velocity decreased 42 percent, from 72 plus or minus 7 to to 41 plus or minus 4 mm/sec (P less than 0.02); ejection fraction decreased 13 percent, from 0.68 plus or minus 0.01 to 0.59 plus or minus 0.01; and end-diastolic bolume increased 28 percent, from 79 plus or minus 11 to 102 plus or minus 9 ml/m2 (P less than 0.05). The preejection period and the ratio between preejection period and left ventricular ejection time significantly increased with progessive dose increments. There was no correlation between blood level of propranolol and improved work performance. Exercise tolerance was maximally improved with doses of 80 to 160 mg/day. At higher dose levels left ventricular function deteriorated and exercise work decreased. Noninvasive assessment of left ventricular function proved more valuable than determination of drug blood levels in managing patients with angina pectoris and provided a guide to optimal adjustment of dosage.

Adult↗
PubMed1975

Metabolic and hemodynamic consequences of mannitol following myocardial anoxia.

The mechanism of action of hyperosmolal mannitol was evaluated by hemodynamic and metabolic studies in 79 isovolumic nonrecirculating paced perfused rat hearts during sequential 15-min periods of aerobic, anoxic, and reoxygenated perfusion. Hyperosmolality induced by addition of mannitol significantly decreased myocardial water content (wet/dry wt ratio). It improved recovery of hemodynamic function during reoxygenation. With isomolal perfusion (290 mosmol/kg) left ventricular systolic peak pressure (LVSP) decreased 32% (127 +/- 5 to 86 +/- 6 mmHg) and maximum dP/dt fell 50% (3,513 +/- 328 to 1,758 +/- 172 mmHg/s) during the postanoxic recovery period. With hyperosmolal perfusion (350 mosmol/kg), LVSP decreased 23% (132 +/- 5 to 102 +/- 7 mmHg) and dP/dt fell 21% (3,817 +/- 215 to 2,998 +/- 234 mmHg/s) (P less than .01). Hyperosmolal perfusion did not affect postanoxic total coronary flow, lactate and glucose metabolism, tissue glycogen, creatine phsophate, or adenine nucleotide concentrations. Coronary perfusion with hypersmolal solution aided recovery, enhanced postanoxic myocardial performance, and minimized tissue swelling. The most tenable explanation for the locus of action of hyperosmolal mannitol during anoxia under our experimental conditions is its direct effect on myocardial water content.

Adenosine Triphosphate↗
PubMed1975

Effects of mannitol on cardiac ultrastructure and microcirculation following anoxia.

Electron microscopic and microcirculatory effects of hyperosmolal mannitol were evaluated in the isolated perfused isovolumic rat heart. Specimens for ultrastructural examination were obtained in 26 experiemnts after 15 min of sequential aerobic, anoxic, and reoxygenated perfusion using an isosmolal perfusate of Krebs-Ringer-Henseleit bicarbonate buffer (KRB) (osmolality equals 290 mosmol/kg) vs. a hyperosmolal solution of KRB + mannitol (equals 350 mosmol/kg). No significant changes were noted during aerobic perfusion. Anoxic hearts perfused with isosmolal KRB demonstrated the most severe ultrastructural alterations including: mitochondrial swelling with disruption of cristae, myofibrillar fusion and contraction bands, and subsarcolemmal edema and vacuolization. These subcellular changes were not only partially reversed by oxygenated isosmolal perfusion but were significantly reversed during both the anoxic and reoxygenation perfusion periods with mannitol added. Following silicone rubber injection of the microcirculation, only focal capillary endothelial cell swelling was noted, and no difference in arteriolar or capillary filling was observed with either perfusate. Thus, mannitol significantly reversed the postanoxic ultrastructural changes consistently observed in the absence of increased osmolality. No gross effect on vascular patency could be demonstrated.

Animals↗
PubMed1975

Cerebrospinal fluid acidosis complicating therapy of experimental cardiopulmonary arrest.

Cardiopulmonary resuscitation (CPR) may be followed by slow recovery of brain function. The possible role of bicarbonate therapy was assessed by analysis of arterial blood and cerebrospinal fluid (CSF) in 20 dogs during cardiac arrest and CPR. Samples were taken in the control period and every 5 minutes post-arrest of 20 minutes. Group I received no post-arrest CPR. Arterial pH fell from 7.37 to 7.31 (P less than 0.01) and CSF pH from 7.34 to 6.94 (P less than 0.001). Arterial pCO2 rose from 39 to 65 mm Hg (P less than 0.005) and CSF pCO2 increased from 47 to 123 (P less than 0.02). With CPR alone (group II) arterial pH decreased from 7.39 to 7.19 (P less than 0.005), while arterial pCO2 and CSF pH and pCO2 were undhanged. CPR with bicarbonate therapy (mEq = weight in kg times 0.43 times 1.1 mEq/min of arrest) given every 5 minutes (group III), resulted in a rise in arterial pH from 7.41 to 7.81 (P less than 0.02). Excess bicarbonate administration during CPR may result in a marked dissociation between arterial and CSF pH as a consequence of rapid CO2 diffusion across the blood-brain barrier. Large ampounts of NaHCO3 given during CPR may contribute to post-CPR cerebral depresssion.

Acid-Base Equilibrium↗
PubMed1975

Electrocardiographic criteria for the diagnosis of left anterior fascicular block. Left axis deviation and delayed intraventricular conduction.

The two current criteria for diagnosis of left anterior fascicular block (LAFB) were evaluated; they are marked left axis deviation (LAD) and a delay in the time of inscription of the intrinsicoid deflection (ID) in lead aVL asynchronous to V6. From 400 electrocardiograms with a LAD of --30 degrees or greater, 62 percent showed asynchronous activation of the left ventricle. There was only a general relationship between the degree of LAD and delayed ID in aVL. The incidence of delayed ID in aVL was as follows: 2 percent with mean frontal QRS axis at 0 degrees; 9 percent at --15 degrees; 41 percent at --30 degrees; 69 percent at --45 degrees; 82 percent at --60 degrees; and 100 percent at --75 degrees or greater. The lack of correlation between both criteria in many instances questions their validity. The LAD alone should not be considered synonymous with LAFB. Recognition of delayed inscription of the ID in aVL is a useful supplemental criterion for diagnosis.

Bundle-Branch Block↗
PubMed1975

Time, place, event of sudden death.

Sudden death, known since antiquity, is almost always due to cardiovascular disorder, but not exclusively to coronary artery disease. It is postulated that two processes, action of pre-existing risk factors (enlarged heart, abnormal conduction, extra systoles, ischemia) and new, untoward events (acute infarction or ischemia) culminate in the catastrophic event. Sudden death is apparently most likely during waking hours; sleep is a lesser risk. Which subjects are at greatest risk and which circumstances are most dangerous remain unknown and are important topics for further investigation.

Adolescent↗