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Biomedical subjects

P G Camici

Publications and source records attributed to P G Camici.

At least 109 records · Page 6Linked to original sources
PubMed1995

Effect of aging on myocardial perfusion reserve.

UNLABELLED: Myocardial perfusion reserve (hyperemic divided by basal myocardial blood flow) describes vasodilator responsiveness of coronary-resistive vessels. The effect of aging and gender on myocardial perfusion reserve remains controversial. METHODS: We studied 56 normal volunteers (21 women, 35 men; aged 50 +/- 20 yr, range 21-86 yr) with 15O-water PET to measure myocardial blood flow during basal and hyperemic states with intravenous dipyridamole (0.56 mg/kg, n = 46) or adenosine (140 micrograms/kg/min, n = 10). For comparative analysis, patients were grouped according to age: < 30 yr (n = 11), 30-49 yr (n = 18), 50-69 yr (n = 15) and > or = 70 yr (n = 12). RESULTS: Overall, basal flow was 1.00 +/- 0.26 ml/min/g and hyperemic flow was 3.31 +/- 1.38 ml/min/g, resulting in a myocardial perfusion reserve of 3.38 +/- 1.35. There was an increase in basal flow with age (r = 0.45, p < 0.025), although hyperemic flow was only lower in patients > or = 70 yr, causing a significant reduction in myocardial perfusion reserve: 3.54 +/- 0.96 in < 30 yr, 4.23 +/- 1.35 in 30-49 yr, 3.51 +/- 1.21 in 50-69 yr and 1.94 +/- 0.46 in > or = 70 yr (p < 0.05 versus all groups < 70 yr). CONCLUSION: Myocardial blood flow during basal and hyperemia conditions are roughly comparable up to 60 yr of age. Above this age, there is significant increase in basal flow associated with an increase in systolic blood pressure. Above 70 yr, there is a significant reduction in hyperemic flow, and thus myocardial perfusion reserve independent of hemodynamic response to vasodilator stress.

Adenosine↗
PubMed1994

Effect of verapamil on absolute myocardial blood flow in hypertrophic cardiomyopathy.

Angina, despite angiographically normal coronary arteries, is a common symptom in patients with hypertrophic cardiomyopathy (HC). Verapamil has been shown to ameliorate silent myocardial perfusion defects documented by thallium-201 in patients with HC. The aim of this study was to investigate the effects of verapamil on absolute regional myocardial blood flow and flow reserve, measured by positron emission tomography (PET) in patients with HC. Echocardiography, exercise stress testing, and measurements of myocardial blood flow at rest and after administration of intravenous dipyridamole (0.56 mg/kg) were undertaken in 20 patients with HC at baseline study and 8 +/- 2 weeks after double-blind randomization to either slow-release verapamil 240 mg or placebo once daily. During treatment, resting myocardial blood flow in the interventricular septum was 0.81 +/- 0.23 versus 0.96 +/- 0.42 ml/min/g in the placebo and verapamil group, respectively (p = NS between groups and when compared with respective baseline study); resting myocardial blood flow in the left ventricular free wall was 0.67 +/- 0.17 versus 0.74 +/- 0.45 ml/min/g, respectively (p = NS). After dipyridamole infusion, myocardial blood flow in the interventricular septum was 1.42 +/- 0.52 versus 1.92 +/- 1.23 ml/min/g (p = NS between groups and when compared with respective baseline study); myocardial blood flow in the left ventricular free wall was 1.25 +/- 0.41 versus 1.68 +/- 1.37 ml/min/g, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Central nervous pathways mediating angina pectoris.

The central nervous pathways of angina pectoris have never been identified in vivo in man. We used positron emission tomography to examine the changes in regional cerebral blood flow associated with angina pectoris. Dynamic positron emission tomography with 15O-labelled water was used in 12 patients with angina and angiographically proven coronary artery disease to measure regional cerebral blood flow changes during angina induced by intravenous dobutamine. All subjects had typical retrosternal chest pain accompanied by ischaemic electrocardiographic changes during dobutamine infusion. Compared to the resting state, angina was associated with increased regional cerebral blood flow in the hypothalamus (percentage change in regional cerebral blood flow +6.5 and Z score 7.2) periaquaductal grey (+2.6 and 4.0), bilaterally in the thalamus (left: +2.7 and 4.3; right +3.7 and 4.7) and lateral prefrontal cortex (left +11.5 and 7.6; right +8.5 and 7.8) and left inferior anterocaudal cingulate cortex (+9.4 and 6.6). In contrast, it was reduced bilaterally in the mid-rostrocaudal cingulate cortex (left -3.7 and 6.3; right -4.7 and 4.6) and fusiform gyrus (left -3.2 and 4.0; right -3.3 and 3.7), right posterior cingulate (-3.9 and 5.8) and left parietal cortices (-4.8 and 6.3). Several minutes after stopping dobutamine infusion, when the patients no longer experienced angina and the electrocardiographic changes had resolved, thalamic, but not cortical activation could be seen. We propose that the central structures activated constitute the pathways for perception of anginal pain and that the thalamus may act as a gate to afferent pain signals, with cortical activation being necessary for the sensation of pain. This method of investigation may form a basis for research into anomalies of visceral pain perception such as silent myocardial ischaemia.

Adult↗
PubMed1994

Relation between myocardial blood flow and the severity of coronary-artery stenosis.

BACKGROUND: We assessed the relation between the severity of stenosis in a coronary artery and the degree of impairment of myocardial blood flow. Studies in laboratory animals have shown that as the degree of coronary-artery stenosis increases, the maximal coronary flow measured after maximal vasodilation progressively decreases, with a concomitant decrease in basal flow. However, this relation has not been carefully documented in humans through measurement of myocardial blood flow. METHODS: We studied 35 patients with single-vessel coronary artery disease and normal left ventricular function and 21 age-matched controls. Regional myocardial blood flow in the area supplied by the stenosed artery was measured by positron-emission tomography with oxygen-15-labeled water while the subject was at rest (basal flow) and during hyperemia induced by the intravenous administration of the vasodilator adenosine (140 micrograms per kilogram of body weight per minute) or dipyridamole (0.56 mg per kilogram). RESULTS: The mean (+/- SD) basal myocardial blood flow was 1.14 +/- 0.42 ml per minute per gram of tissue in the patients and 1.13 +/- 0.26 ml per minute per gram in the controls; during hyperemia, myocardial flow was 2.10 +/- 1.16 and 3.37 +/- 1.25 ml per minute per gram (P < 0.001), respectively. Basal flow was unchanged regardless of the severity of stenosis, expressed as a percentage of the diameter of the affected vessel (range of degrees of stenosis, 17 to 87 percent). In contrast, flow during hyperemia correlated inversely and significantly with the degree of stenosis and correlated directly with the minimal luminal diameter. The coronary vasodilator reserve (defined as the ratio of flow during hyperemia to flow at base line) began to decline when the degree of stenosis was about 40 percent and approached unity when stenosis was 80 percent or greater. CONCLUSIONS: In humans, basal myocardial blood flow remains constant regardless of the severity of coronary-artery stenosis. However, during hyperemia, flow progressively decreases when the degree of stenosis is about 40 percent or more and does not differ significantly from basal flow when stenosis is 80 percent or greater.

Adult↗
PubMed1994

Adrenergically mediated coronary vasoconstriction in patients with syndrome X.

Several studies have shown that coronary vasodilator reserve is impaired in some patients with chest pain and angiographically normal coronary arteries. In a subgroup of these patients, who additionally show ST depression on the electrocardiogram during exercise and are generally labelled as having Syndrome X, the impairment of coronary flow reserve is associated with metabolic and functional signs consistent with an increased sympathetic drive. The aim of the present investigation was to ascertain whether the impairment of coronary vasodilator reserve in patients with Syndrome X is due to adrenergically mediated vasoconstriction of coronary microcirculation. Myocardial blood flow (MBF), at baseline and following intravenous infusion of dipyridamole (0.56 mg/kg over 4 minutes), was measured by means of 13N-ammonia and dynamic positron emission tomography in 10 females (mean age 52 +/- 8 years) with a chest pain history, ST-segment depression during exercise, and angiographically normal coronaries. The first MBF study was performed while the patients were off therapy; a repeat MBF study was performed following 1 week of treatment with the alpha-1 blocker doxazosin (2 mg/day). Off therapy MBF was 1.13 +/- 0.25 ml/min/g at baseline and increased to 2.35 +/- 0.66 ml/min/g following dipyridamole. Coronary vasodilator reserve (dipyridamole/baseline MBF) was 2.18 +/- 0.56. During treatment with doxazosin, baseline MBF was not different from the control value (1.25 +/- 0.50 ml/min/g), while added dipyridamole significantly increased MBF to 3.52 +/- 1.20 ml/min/g (p < 0.01 vs. off therapy). Coronary vasodilator reserve was significantly increased (2.91 +/- 0.92, p < 0.01 vs. control value) by doxazosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Coronary vasodilator reserve, pain perception, and sex in patients with syndrome X.

BACKGROUND: It remains unclear whether myocardial ischemia due to coronary microvascular dysfunction is the cause of chest pain in syndrome X (chest pain, ischemic-like stress ECG despite angiographically normal coronary arteries). To assess the function of the coronary microcirculation and its relation to pain perception, we measured myocardial blood flow (MBF) and coronary vasodilator reserve (CVR) in 29 patients with syndrome X and 20 matched normal control subjects. METHODS AND RESULTS: MBF at rest and after intravenous dipyridamole (0.56 mg.kg-1 over 4 minutes) was measured using positron emission tomography with H2(15)O. CVR was calculated as MBFdipyridamole/MBFrest. ECG changes and chest pain after dipyridamole in syndrome X were compared with those in 35 patients with coronary artery disease (CAD). Resting and postdipyridamole MBFs were homogeneous throughout the left ventricle in syndrome X patients and control subjects. MBF was 1.05 (0.25), mean (SD) versus 1.00 (0.22) mL.min-1.g-1 (P = NS) at rest and 2.73 (0.81) versus 3.00 (1.00) mL.min-1.g-1 (P = NS) after dipyridamole in patients and control subjects, respectively. CVRs were 2.66 (0.76) and 3.06 (1.08) (P = NS) and after correction of resting MBF for rate-pressure product were 2.35 (0.83) and 2.34 (0.90) (P = NS) in patients and control subjects, respectively. Female syndrome X patients had higher resting MBF than males, at 1.18 (0.20) versus 0.88 (0.19) mL.min-1.g-1 (P < .001). Chest pain after dipyridamole occurred in syndrome X as frequently as in CAD (21/29 versus 22/35, P = NS). CONCLUSIONS: When patients with syndrome X are compared with control subjects, no differences are found in MBF either at rest or after dipyridamole, despite syndrome X patients experiencing chest pain after dipyridamole to the same extent as patients with CAD. These findings, together with the absence of any relation among MBF, chest pain, and ECG changes under stress, cast further doubt on ischemia as the basis of the chest pain, at least in the majority of syndrome X patients.

Adult↗
PubMed1994

[Microcirculation and remodelling].

Acute myocardial infarction can produce alterations in the topography of the left ventricle both in the infarcted and remote areas. These changes as a whole, have been termed ventricular remodelling. Attention has been focused on myocyte alterations due to the remodelling process, but the myocardial wall also contains fibroblasts, which produce collagen and elastin fibers, and endothelial and smooth muscle cells which are the main constituents of the vascular wall. In left ventricular hypertrophy, a form of myocardial remodelling, structural changes of myocytes, cardiac interstitium as well as the coronary microcirculation have been found (vascular remodelling). In vivo, the function of coronary microcirculation can be evaluated by measuring myocardial blood flow and coronary reserve. In fact the study of coronary reserve in patients with left ventricular hypertrophy disclosed microcirculatory dysfunction which probably represents the functional counterpart of the structural changes already described. Positron emission tomography (PET) can noninvasively quantitate myocardial blood flow and coronary reserve in humans. Recently studies with PET disclosed microcirculatory alterations also in patients with coronary artery disease (CAD) in the absence of gross myocardial hypertrophy. In particular, after myocardial infarction, coronary vasodilator capacity has been shown to be impaired not only in the infarcted areas but also in the remote ones subtended by angiographically normal vessels. A blunted coronary reserve has been identified with PET also in remote regions from ischemia in patients with stable angina and single vessel CAD.

Angina Pectoris↗
PubMed1993

Altered coronary vasodilator reserve and metabolism in myocardium subtended by normal arteries in patients with coronary artery disease.

OBJECTIVES: The aim of this study was to investigate coronary vasodilator reserve and metabolism in myocardium subtended by angiographically normal arteries remote from ischemia. BACKGROUND: After infarction, structural and functional changes occur in remote myocardium often subtended by normal arteries. Whether changes occur in regions remote from ischemic but noninfarcted myocardium is unknown. METHODS: Coronary vasodilator reserve was measured with positron emission tomography in 12 patients with single-vessel disease using intravenous dipyridamole (0.56 mg/kg for 4 min). In another 10 patients, simultaneous arterial/great cardiac vein catheterization was performed during atrial pacing to measure myocardial metabolism in regions subtended by diseased or normal arteries. RESULTS: Basal myocardial blood flow in stenosis-related regions was comparable to that in remote regions but was lower after dipyridamole administration (1.73 +/- 0.91 vs. 2.89 +/- 0.93 ml/min per g, p < 0.01), giving coronary vasodilator reserve values of 1.80 +/- 0.82 and 2.73 +/- 0.89 (p < 0.01). In normal control subjects, basal myocardial blood flow was 0.92 +/- 0.13 and 3.67 +/- 0.94 ml/min per g in the basal state and after dipyridamole (both p < 0.05 vs. values in remote regions), and coronary vasodilator reserve was 4.07 +/- 0.98 (p < 0.01) vs. values in remote regions). During pacing there was net lactate release in diseased regions (-18 +/- 27%, p < 0.05 vs. values in remote regions and control subjects) and extraction in remote regions (38 +/- 17%) and in normal control subjects (26 +/- 11%). Glucose and alanine extraction were increased in diseased (8 +/- 6% and 6 +/- 6%) and remote regions (6 +/- 3% and 4 +/- 3%), compared with values in normal control subjects (2 +/- 3% and -1 +/- 3%, both p < 0.05 vs. diseased and remote regions). CONCLUSIONS: Coronary vasodilator reserve is reduced and glucose and alanine metabolism is abnormal in regions subtended by normal arteries remote from ischemic but noninfarcted myocardium.

Aged↗
PubMed1993

Assessment of myocardial viability and the role of surgery.

The importance of accurately predicting functional recovery of the myocardium has become clear with the advent of interventional techniques for coronary revascularization. Detection of hibernating myocardium (reversibly dysfunctional myocardial segments subtended by stenosed arteries) has been approached by techniques that assess different characteristics of this condition, such as contractile reserve, membrane integrity, and metabolic activity. The standard for detecting viable myocardium is considered to be metabolic imaging with positron-emission tomography using the glucose analogue 18F-fluorodeoxyglucose, which makes it possible to quantitate regional glucose utilization in myocardium. However, recently, a new approach has been proposed based on the use of 15O-labeled water, which does not require metabolic imaging and appears to offer advantages in terms of scanning time and quantitation of viable tissue.

Cardiomyopathies↗
PubMed1993

Evidence for a systemic defect of resistance-sized arterioles in hypertrophic cardiomyopathy.

BACKGROUND: To investigate whether the abnormalities of coronary arterioles observed in association with hypertrophic cardiomyopathy represent a generalized phenomenon, both forearm and coronary vasodilator reserve were measured in 12 patients with hypertrophic cardiomyopathy. METHODS: Forearm vasodilator reserve was evaluated by measuring minimal forearm vascular resistance (Rmin, the ratio of mean intra-arterial pressure to peak forearm blood flow measured by venous plethysmography) under conditions of maximal postocclusive reactive hyperemia. RESULTS: In a subgroup (n = 5) of patients, the intra-arterial infusion of sodium nitroprusside combined with arterial occlusion did not produce additional vasodilation, indicating that the ischemic stimulus was indeed maximal. Coronary reserve was quantitated by measuring left ventricular blood flow (13N-ammonia and positron emission tomography) and coronary resistance at baseline and after intravenous dipyridamole (0.56 mg/kg). Rmin was significantly greater in patients than in a group of age- and sex-matched controls. The percentage change in coronary resistance after dipyridamole was significantly related to Rmin, whereas no correlation was found between change in coronary resistance and individual septal thickness values. CONCLUSIONS: Independent of cardiac hypertrophy, systemic and coronary arterioles of patients with hypertrophic cardiomyopathy are affected by an abnormality that may contribute to the clinical evolution of this syndrome.

Adult↗
PubMed1993

An additional marker for familial hypertrophic cardiomyopathy?

BACKGROUND: Family screening for hypertrophic cardiomyopathy using conventional techniques yields some equivocal cases. Although mutations in the beta-cardiac myosin heavy-chain gene (MYH7) have been demonstrated in some patients, additional diagnostic methods are desirable to clarify the equivocal cases until the full genetic spectrum is characterized. Because coronary flow reserve is reduced in patients with typical hypertrophic cardiomyopathy independent of the severity of left ventricular hypertrophy, this measurement may help to identify patients with equivocal features of the disease. METHODS: Coronary flow reserve was measured in two subjects: one with a MYH7 mutation but without typical diagnostic features of hypertrophic cardiomyopathy, and one with borderline left ventricular hypertrophy but no mutation in the MYH7 gene. Both subjects underwent screening for hypertrophic cardiomyopathy because of a family history of the disease. Positron-emission tomography was performed to measure myocardial blood flow (MBF) with oxygen-15 labeled water. MBF was measured at baseline and during coronary vasodilatation obtained by intravenous dipyridamole (0.56 mg/kg body weight infused over 4 minutes). Coronary flow reserve was expressed as the ratio MBF-dipyridamole/MBF-baseline. RESULTS: Coronary flow reserve was 1.69 and 1.12 in the two subjects. Both of these values are 2 SD below that (3.87 +/- 1.08) measured in 17 normal subjects using the same method. CONCLUSIONS: Noninvasive quantification of coronary flow reserve by positron-emission tomography may have a role in identifying patients with equivocal hypertrophic cardiomyopathy and should be further explored.

Adolescent↗
PubMed1993

Metabolic and hemodynamic effects of insulin on human hearts.

Myocardial muscle is considered to be a target tissue for insulin action, but direct measurements of insulin's effects on cardiac hemodynamics and intermediary metabolism in humans are scarce. We combined great cardiac vein (GCV)/arterial catheterization with the euglycemic insulin clamp technique and thermodilution in six healthy middle-aged (53 +/- 2 yr) volunteers. In the fasting state, the myocardium extracted free fatty acid (FFA), lactate, pyruvate, glycerol, and beta-hydroxybutyrate (6.4 +/- 0.8, 6.2 +/- 1.0, 0.58 +/- 0.12, 0.44 +/- 0.15, and 11 +/- 2 mumol/min, respectively) and consumed 0.26 +/- 0.02 mmol/min oxygen. As fasting plasma insulin (73 +/- 6 pmol/l) was raised and clamped at 503 +/- 16 pmol/l for 100 min while maintaining euglycemia (approximately 5 mmol/l), arterial levels of lactate and pyruvate rose (by 121 and 159%, respectively), whereas FFA, glycerol, and beta-hydroxybutyrate fell (by 69, 48, and 85%, respectively, all P < 0.001). Correspondingly, net myocardial uptake of glucose, lactate, and pyruvate increased to 18.9 +/- 3.5, 32.0 +/- 2.3, and 2.7 +/- 0.5 mumol/min, respectively, whereas net extraction of circulating FFA, glycerol, and beta-hydroxybutyrate was abolished (all P < 0.001). The stimulation of lactate and pyruvate uptake was the result of both increased arterial supply and enhanced myocardial extraction ratio (from 19 +/- 3 to 51 +/- 6% for lactate, from 26 +/- 5 to 44 +/- 5% for pyruvate, P < 0.001 for both). This shift from fat to carbohydrate fuel usage occurred in the absence of changes in oxygen consumption, heart rate, GCV blood flow, aortic pressures, coronary vascular resistance, and left ventricular end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1992

Hibernation and myocardial ischemia: clinical detection by positron emission tomography.

Regions of myocardium supplied by severely diseased epicardial arteries may develop chronic ischemia at rest and exhibit reduced contractility, contributing to a reduction in global left ventricular function. However, after revascularization, contractility in these regions may return to normal. These regions of asynergy are described as "hibernating myocardium." Such myocardium in which normal contractility may be restored often coexists with areas of infarcted, or scar, tissue, leading to the definition of hypoperfused hibernating myocardium as viable myocardium. It is important to identify viable myocardium, as revascularization of these areas should lead to the greatest improvement in left ventricular function and, thus, improvement in survival. Positron emission tomography is the best noninvasive method for quantifying regional myocardial blood flow and metabolism. Using 18F-fluorodeoxyglucose, which measures myocardial glucose utilization, it is possible to identify myocardial tissue that is hypoperfused at rest with preserved or increased glucose uptake. This mismatch of blood flow to metabolism has a high predictive accuracy in the recovery of contractile function. In order to reduce the need for metabolic imaging in documenting myocardial viability, a regional index of perfusable tissue derived from imaging with 15O water has been recently developed that also allows the quantification of tissue viability.

Cell Survival↗