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Biomedical subjects

P G Camici

Publications and source records attributed to P G Camici.

120 records · Page 7Linked to original sources
PubMed1992

Regional myocardial deoxyglucose uptake following electrical stimulation of canine efferent sympathetic cardiopulmonary nerves.

OBJECTIVE: The aim was to study the effect of stimulating individual acutely decentralised cardiopulmonary nerves on myocardial uptake of deoxyglucose. METHODS: In 17 open chest anaesthetised dogs the efferent axons of individual decentralised cardiopulmonary nerves were stimulated intermittently throughout 1 h while haemodynamic variables were measured. Tritiated 2-deoxyglucose was injected intravenously at the beginning of stimulation. Atropine was given when a cardiopulmonary nerve with efferent parasympathetic axons was studied. Distribution of label was detected using a multiwire proportional chamber. It was compared to blood concentration of deoxyglucose to permit quantitative mapping of regional myocardial uptake during the stimulation of each nerve. RESULTS: Neural stimulation of most of sympathetic efferent cardiopulmonary nerves increased deoxyglucose uptake in all myocardial tissue. Uptake was greatest in the left ventricle, less in the right ventricle, and least in the left and right atria. Regional myocardial uptake was also observed following individual cardiopulmonary nerve stimulation. Some nerves caused greater uptake than others. Cardiopulmonary nerves which are known to enhance inotropism when stimulated induced little increase of deoxyglucose uptake, whereas other nerves known to exert little positive inotropic effect induced considerable uptake. There was no correlation between haemodynamic changes and deoxyglucose uptake. CONCLUSIONS: It appears that (1) efferent sympathetic axons in one cardiopulmonary nerve can preferentially increase deoxyglucose uptake in specific regions of the myocardium and (2) the mechanisms responsible for enhancement of glucose uptake may differ from those responsible for inotropic responses.

Animals↗
PubMed1992

Coronary reserve and exercise ECG in patients with chest pain and normal coronary angiograms.

BACKGROUND: Coronary vasodilator reserve is reduced in some patients with a history of chest pain and angiographically normal coronary arteries. ECG changes suggestive of myocardial ischemia during exercise also can be demonstrated in a subset of these patients. METHODS AND RESULTS: We have investigated the correlation between coronary vasodilator reserve, assessed with 13N-labeled ammonia and positron emission tomography, and the ECG during exercise stress in 45 patients with a history of chest pain, angiographically normal coronary arteries, and a negative ergonovine test. ST segment depression on the ECG during exercise was present in 29 of 45 patients. Mean resting left ventricular blood flow was 1.04 +/- 0.22 ml.min-1.g-1; it increased to 1.32 +/- 0.47 ml.min-1.g-1 (p less than 0.01 versus baseline value) during atrial pacing and to 2.52 +/- 0.96 ml.min-1.g-1 (p less than 0.01 versus baseline value) after dipyridamole (0.56 mg/kg i.v.). No regional flow defects could be demonstrated in any patient during pacing or after dipyridamole. Myocardial flows after dipyridamole, however, did not show a normal frequency distribution (Kolmogorov-Smirnov test), and two patient populations could be identified. Twenty-nine (67%) patients had a mean left ventricular flow of 3.02 +/- 0.33 ml.min-1.g-1 after dipyridamole (range, 2.13-5.46 ml.min-1.g-1), and 14 (33%) patients had a mean flow of 1.48 +/- 0.29 ml.min-1.g-1 (range, 1.06-2.04 ml.min-1.g-1, p less than 0.01 versus the "high-flow group"). CONCLUSIONS: Approximately one third of patients in our series showed a reduced coronary vasodilator reserve. Although 12 of 14 patients in the "low-flow group" had ST segment depression during exercise stress, 16 of 29 patients in the high-flow group also had ST segment depression during exercise stress. Therefore, despite a good sensitivity (86%) in identifying patients with a blunted increment of coronary flow, the ECG response during exercise stress appears to have a rather low specificity (45%). This suggests that factors other than reduced coronary reserve and myocardial ischemia may play a role in the genesis of the ST segment depression in these patients.

Adult↗
PubMed1992

Assessment of myocardial perfusion, metabolism and pharmacology using positron emission tomography.

Positron emission tomography is a non-invasive radionuclide imaging technique which enables in vivo assessment of regional cardiac function. When used with appropriate radiotracers and kinetic models, it can provide quantitative measurements of myocardial perfusion, metabolism and pharmacology. The development of quantitative measurements should help to decrease much of the ambiguity in the interpretation of data that often occurs. The short half-life of the radionuclides used allows the imaging of more than one function to be performed conveniently within the same scanning session with a low radiation dose to the subject. This integrated approach provides a means for investigating in vivo the physiology and pathophysiology of the human heart.

Adrenergic beta-Antagonists↗
PubMed1991

Coronary hemodynamics and myocardial metabolism in patients with syndrome X: response to pacing stress.

Coronary hemodynamics, myocardial metabolism and left ventricular function at rest and after incremental atrial pacing were evaluated in 12 patients with stress-induced angina and ST segment depression, angiographically normal coronary arteries and no evidence of spasm, generally labeled as syndrome X, and in 10 normal subjects. At baseline study, great cardiac vein flow was comparable in patients and control subjects. During pacing, an equivalent rate-pressure product was reached in the two groups, but the slope of the relation between rate-pressure product and great cardiac vein flow was significantly less steep in patients than in normal subjects (0.0027 vs. 0.0054 ml/mm Hg.beat, p less than 0.001). Nevertheless, the left ventricular ejection fraction was comparable in both groups at rest (66 +/- 6% vs. 71 +/- 7%, p = NS) and during pacing (71 +/- 7% vs. 66 +/- 5%, p = NS). At baseline study, myocardial glucose extraction was more efficient in patients with syndrome X (p less than 0.05), but net myocardial exchange of pyruvate and alanine was, respectively, smaller and greater than in control subjects. Lactate was extracted to a similar extent in the two groups and in no instance was net lactate release observed during pacing or recovery. During pacing and recovery, patients with syndrome X showed net pyruvate release, unlike the control subjects in whom net pyruvate exchange was positive. In addition, patients with syndrome X continued to show net myocardial extraction of alanine during spacing and recovery, whereas normal subjects produced alanine throughout the study. Myocardial carbohydrate oxidation increased significantly during maximal pacing in normal subjects but not in patients, in whom it always remained below (p less than 0.01) the concurrent rate of myocardial uptake of carbohydrate equivalents (glucose, lactate, pyruvate, alanine). Myocardial energy expenditure was significantly lower in patients than in control subjects at maximal rate-pressure product levels (p less than 0.01). The metabolic pattern in patients with syndrome X therefore is not consistent with classic ischemia, although differences in the net exchange of circulating substrates (glucose, pyruvate, alanine) can be demonstrated. Thus, in patients with syndrome X, the symptoms, electrocardiographic signs and impairment in the increase in great cardiac vein flow during pacing coexist with preserved global and regional left ventricular function and myocardial energy efficiency.

Angina Pectoris↗
PubMedDate not supplied

Investigation of myocardial metabolism for the study of the pathophysiology of cardiac disease.

Many variables, including food ingestion, circulating hormone, and the cardiac work load, affect myocardial metabolism. Important changes in myocardial metabolism are associated with myocardial ischemia. The study of myocardial metabolism by means of different invasive and noninvasive techniques allows a better understanding of both cardiac physiology and pathophysiology in humans.

Humans↗
PubMedDate not supplied

Evaluation of the extent and timing of the coronary hyperemic response to dipyridamole: a study with transesophageal echocardiography and positron emission tomography with oxygen 15 water.

Coronary flow reserve may be measured with Doppler-derived coronary blood-flow velocity or scintigraphic assessment of myocardial perfusion. The purpose of this study was to compare coronary flow velocity and perfusion measures of flow reserve with respect to their extent and time course. Coronary flow velocity reserve in the proximal left anterior descending coronary artery measured by pulsed-wave Doppler at transesophageal echocardiography, with measures of perfusion reserve obtained in the corresponding territory, were measured by a standard O15 water technique at positron emission tomography. Eighteen male volunteers underwent both tests on different days in random order, with dipyridamole stress (0.56 mg/kg). After correction of resting flow and perfusion measurements to a standard cardiac workload (to compensate for heterogeneity in hemodynamics between the two studies), coronary flow reserve was calculated as the ratio between dipyridamoleand corrected resting flow. The uncorrected perfusion reserve measured by positron emission tomography was 3.7 +/- 1.2, compared with a corrected perfusion reserve of 2.3 +/- 0.7. This correlated with a corrected flow velocity reserve of 2.9 +/- 1.0 at transesophageal echocardiography (R = 0.92; p < 0.001). The mean difference between these results was 0.58 +/- 0.41; discrepant results occurred at higher flows, in the presence of discordant blood pressure responses to stress, and because of intersubject variations in the timing of the peak coronary flow response, which were detected by continuous monitoring at transesophageal echocardiography. Measurement of coronary flow reserve at transesophageal echocardiography correlates well with measurements at positron emission tomography, and discrepancies are minimized if measurements are taken at the same time after dipyridamole.

Adult↗
PubMedDate not supplied

The contribution of positron emission tomography to the study of ischemic heart failure.

Cardiac imaging with positron emission tomography offers unrivaled sensitivity and specificity to probe cardiovascular physiology in health and disease. The use of positron emission tomography to noninvasively measure regional myocardial blood flow and assess myocardial viability in patients with ventricular dysfunction and coronary artery disease has contributed greatly to our understanding of the pathophysiology of ischemic heart failure. The advances and the need for further studies to establish both the natural history of such ventricular dysfunction and the role of coronary revascularization are discussed.

Coronary Circulation↗
PubMedDate not supplied

Myocardial hibernation vs repetitive stunning in patients.

Myocardial hibernation is a state of persistently impaired left ventricular function in patients with coronary artery disease that was thought to be caused by a chronic reduction in resting myocardial blood flow in a segment subtended by a diseased coronary artery. However, recent studies using positron emission tomography have demonstrated that absolute myocardial blood flow (ml/min/g) to hibernating myocardium is within normal limits in most patients. If resting flow is not reduced, one must therefore suspect an alternative "trigger" for hibernation that is still a consequence of coronary artery disease and ischemia. We suspect that hibernating myocardium may be the result of repetitive myocardial stunning. Myocardial stunning is the reversible contractile dysfunction occurring after a period of myocardial ischemia that persists for a period of time despite the return of blood flow to normal. Myocardial stunning has been demonstrated in humans in the setting of thrombolysis, coronary angioplasty, coronary artery bypass surgery, and coronary artery spasm. Furthermore, stunning has been demonstrated after exercise in patients with coronary artery disease, and recent studies have provided evidence that repetitive episodes of exercise-induced ischemia can lead to cumulative and prolonged left ventricular dysfunction.

Coronary Circulation↗
PubMedDate not supplied

Myocardial presynaptic and postsynaptic autonomic dysfunction in hypertrophic cardiomyopathy.

Although hypertrophic cardiomyopathy (HCM) is genetically determined, several other factors, including autonomic dysfunction, may play a role in the phenotypic expression. A recent study using positron emission tomography with [11C]CGP 12177 ([11C]CGP) demonstrated that beta-adrenoceptor (betaAR) density is reduced in HCM and is correlated with disease progression. This present study tested the hypothesis that this downregulation is associated with reduced catecholamine reuptake (uptake 1) by myocardial sympathetic nerve terminals leading to increased local norepinephrine concentration. Myocardial presynaptic catecholamine reuptake was assessed by measuring the volume of distribution (Vd) of the catecholamine analogue [11C]hydroxyephedrine ([11C]HED) in 9 unrelated HCM patients aged 45+/-15 years. The maximum number of binding sites (Bmax) for myocardial betaAR density was measured in 13 unrelated HCM patients aged 40+/-12 years using the nonselective beta blocker [11C]CGP. Six patients were studied with both [11C]HED and [11C]CGP. Comparison was made with two groups of healthy control subjects for each ligand ([11C]HED, n=10, aged 35+/-8 years; [11C]CGP, n=19, aged 44+/-16 years). Myocardial Vd of [11C]HED (33.4+/-4.3 mL/g tissue) and betaAR density (7.3+/-2.6 pmol/g tissue) were significantly reduced in HCM patients compared with control subjects (71.0+/-18.8 mL/g tissue, P<.001, and 10.2+/-2.9 pmol/g tissue, P=.008, respectively). These results are consistent with our hypothesis that myocardial betaAR downregulation in HCM is associated with an impaired uptake-1 mechanism and hence increased local catecholamine levels.

Adult↗