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Biomedical subjects

D Cianflone

Publications and source records attributed to D Cianflone.

At least 37 records · Page 2Linked to original sources

[Psychological stress as precipitating factor of the acute manifestations of ischemic cardiopathy].

Psychological stress may play an important role as a risk factor for coronary heart disease (CHD). Psychological stress consists of different components whose diverse role in the onset of the acute manifestations of CHD is still not clear. We studied 80 patients with acute CHD (56 with unheralded myocardial infarction, 24 with unstable angina, mean age 55 +/- 9 years, 55 men) vs 80 controls (mean age 50 +/- 9 years, 52 men) admitted for an acute traumatic event. We proposed to both groups these questionnaires: a retrospective self and etero-evaluation of the degree of psychological stress; the modified Maastricht questionnaire (MMQ) that evaluates psychic and physical manifestations of psychological stress in the period preceding admission; the social support questionnaire (SSQ); the life event assessment that evaluates frequency and importance of life events in the year preceding admission. Psychological stress index was greater in patients (self-evaluation = 7.1 +/- 2.4; etero-evaluation = 7.4 +/- 2.3; MMQ = 91 +/- 30.8) than controls (self-evaluation = 4.3 +/- 2.3; etero-evaluation = 4.3 +/- 2.4; MMQ = 58.6 +/- 32.5; p < 0.001 for all questionnaires). The perception of strong social isolation was greater in patients (SSQ = 29.8 +/- 11.8) than controls (SSQ = 23.8 +/- 9.6; p < 0.001). Painful life events were more numerous in patients (10.7 +/- 2.3) than controls (8.2 +/- 3.4; p < 0.05) and perceived in a more negative way (patients = 12.7 +/- 4.1 vs controls = 10.2 +/- 3.8; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗

[Interactions between atherosclerosis and ischemic stimuli in the pathogenesis of acute coronary syndromes].

Until a few years ago coronary atherosclerosis was thought to be a slowly progressive disease eventually leading to total coronary occlusion and myocardial infarction. Recent angiographic studies have shown, instead, that mild or moderate coronary stenoses have the highest risk of causing acute coronary syndromes when complicated by thrombus formation which, in turn, appears to be due to a complex interaction between the atherosclerotic background and acute ischemic stimuli. The tendency of the atherosclerotic background to develop thrombosis may be different in different patients, as indicated by the observation that the risk factor profile of patients who present with chronic coronary syndromes is different from that of patients who present with acute syndromes. The acute ischemic stimuli so far identified are: a sudden local thrombogenic stimulus; a transient systemic increase in systemic pro-coagulant activity; a transient increase in proximal and/or distal coronary tone. The recent observation of inflammatory cells activation, including T-lymphocytes, in patients with acute ischemic syndromes raises the intriguing possibility that a specific antigenic stimulus may play an important pathogenetic role.

Arteriosclerosis↗

[Therapy of microvascular angina].

The treatment of microvascular angina (anginal pain resulting from myocardial ischemia due to dysfunction of small coronary arteries) is empiric and often ineffective at present. The poor knowledge of the pathophysiologic mechanisms responsible for the microvascular dysfunction and the possible heterogeneous nature of the disease limit the possibility of a rational therapeutic approach to these patients. The failure of traditional antiischemic therapy is confirmed by the frequent unresponsiveness of angina and by the reduced exercise tolerance with administration of sublingual nitrates. Despite that, beta-blockers and calcium-antagonists, when given either alone or in combination, are beneficial in the control of symptoms in some patients. Alternative forms of treatment, based on some pathophysiological hypotheses and clinical observations, include xanthine derivatives, ACE-inhibitors, alpha-blocking agents, imipramine and, in women, oestrogens. The actual clinical usefulness of these drugs, however, is questionable at present, as their efficacy should be evaluated with more adequate studies in the future.

Adrenergic alpha-Antagonists↗

[Mechanisms of coronary microvascular dysfunction].

Abnormal constriction of coronary resistive vessels can induce angina and myocardial ischemia. The possibility that a microvascular vasomotor dysfunction could cause ischemia is in contrast with the well-known traditional notion that a metabolically induced vasodilation could compensate for the effect of an epicardial coronary stenosis. Vasoconstrictor stimuli can plausibly act on vessels situated immediately proximal (prearterioles) to those that can be dilated by ischemia metabolites (arterioles). This functional 2-compartment model of resistive vessels is based on the ability of different substances to cause opposite actions on resistive vessels with different sizes. The possible mechanisms of prearteriolar dysfunction, observed in patients with syndrome X, single vessel disease after a successful PTCA and in a subset of chronic stable patients include: an organic reduction of total vascular section; vascular smooth muscle hyperreactivity to heterogeneous constrictor stimuli; an impaired flow-mediated endothelium-dependent vasodilation (possibly due to a reduced NO and/or EDHF synthesis). The first and third hypothesis can only account for anginal episodes at effort while the second model could explain episodes occurring at rest and without an increase in heart rate. Those mechanisms causing an imbalance between myocardial oxygen supply and demand, induce an increased release of adenosine in order to promote a compensating vasodilation. Adenosine can possibly avoid the occurrence of ischemia but, being a powerful algogenic stimulus, causes pain. It is worth noting that the presence of patchy prearteriolar dysfunction induces areas with excessive release of adenosine. Since total vascular section is extremely large a massive adenosine spill-over can occur with a consequential boosting of algogenic and vasodilatory effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Disease↗

Assessment of residual tissue viability by exercise testing in recent myocardial infarction: comparison of the electrocardiogram and myocardial perfusion scintigraphy.

The assessment of residual myocardial viability in infarcted areas is relevant for subsequent management and prognosis but requires expensive technology. To evaluate the possibility that simple, easily obtainable clinical markers may detect the presence of within-infarct viable tissue, the significance of exercise-induced ST elevation occurring in leads exploring the area of a recent Q wave myocardial infarction was assessed. Twenty-five patients with recent (less than 6 months) myocardial infarction were studied. All had angiographically documented coronary artery disease, diagnostic Q waves (n = 24) or negative T waves (n = 25) on the rest 12-lead electrocardiogram and exhibited during exercise greater than or equal to 1.5 mm ST segment elevation (n = 17) or isolated T wave pseudonormalization (n = 8) in the infarct-related leads. ST-T wave changes were reproduced in all patients during thallium-201 exercise myocardial scintigraphy. A fixed perfusion defect was observed in 24 of the 25 patients. A reversible defect was seen in 16 (94%) of 17 patients who exhibited transient ST elevation during exercise but in only 4 (50%) of the 8 patients who had only T wave pseudonormalization. In conclusion, in patients with recent myocardial infarction, analysis of simple ST segment variables obtained during exercise testing may allow a first-line discrimination of those who may potentially benefit from a revascularization procedure.

Coronary Angiography↗

Intravenous nitroglycerin suppresses exercise-induced arrhythmias in patients with ischaemic heart disease: implications for long-term treatment.

We studied 20 patients with ischaemic heart disease, who consistently developed complex ventricular arrhythmias during exercise testing. Treadmill exercise was performed twice, both during the placebo infusion and then during intravenous administration of nitroglycerin, titrated to reduce systolic blood pressure by 10 mmHg. Exercise duration in those administered placebo was 7.8 +/- 1.7 and 7.9 +/- 1.5 min, respectively (ns); angina developed in five patients and ischaemic ST changes in 10. In those administered nitroglycerin, exercise duration increased to 8.4 +/- 2 min (P less than 0.05). Diagnostic ST segment depression was observed in only two patients and only one had angina. Ventricular arrhythmias, consistently present during both tests on those administered placebo, were dramatically reduced by nitroglycerin in all 20 patients. There were 455 (mean 35.8 +/- 16.8) and 418 (mean 34.4 +/- 11.1) ventricular ectopic beats in the two exercise tests on those administered placebo and 11 in those receiving the nitroglycerin infusion (mean 0.6 +/- 0.1) (P less than 0.001). There were 28 and 29 couplets in those receiving placebo (ns) and none in those receiving nitroglycerin (P less than 0.001). Ventricular tachycardia was present in six and eight patients who received placebo but in none in those administered nitroglycerin (P less than 0.001). Abolition of exercise-induced arrhythmias was maintained during chronic treatment with oral coronary vasodilators. Prevention of exercise-related arrhythmias by nitroglycerin appears a good indicator of their ischaemic origin and may provide valuable information for long-term prophylaxis with oral vasodilators, thus avoiding antiarrhythmic agents with their potential side effects.

Arrhythmias, Cardiac↗

[Morphofunctional changes in the left ventricle of the elderly person and the vulnerability to myocardial necrosis].

In the Western world the percentage of subjects over the age of 60 years is rapidly increasing. Therefore, elderly individuals represent a progressively increasing proportion of patients with ischemic heart disease (IHD), which is the most prevalent disease in this age range. In the elderly both the clinical presentation and the outcome of IHD have some peculiar features which may have important therapeutic implications. The prevalence of both coronary atherosclerosis and uncomplicated angina pectoris increases up to the sixth decade when it reaches a plateau. Conversely, the prevalence of myocardial infarction increases progressively at increasing ages without reaching any plateau at all. These findings indicate that the higher prevalence of myocardial infarction in the elderly is not caused by a worsening of the atherosclerotic background, but rather by a greater prevalence and/or severity of the functional factors such as local smooth muscle hyperreactivity, local thrombotic stimuli and alterations of the systemic thrombosis-thrombolysis equilibrium which are more directly responsible for the irreversible occlusion of a coronary artery branch. Therefore, the prevention of IHD in the elderly should focus mainly on the ischemic stimuli leading to coronary thrombosis rather than on the atherosclerotic background. Another important feature of IHD in the elderly is the high short and medium-term mortality of acute myocardial infarction. This excess of mortality is caused mainly by a much higher incidence of cardiac rupture, which does not appear to be related to the severity of coronary atherosclerosis nor to the infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[The coronary collaterals influence in the recovery phase after exercise-induced myocardial ischemia].

The role of coronary collaterals in conditioning the recovery from exercise-induced myocardial ischaemia has not been investigated. We studied 60 patients (54 men, age 59.3 +/- 6.7 years) with low threshold effort angina and documented coronary artery disease, who underwent repeat exercise testing in 2 consecutive days. On the second day, Thallium 201 stress/rest myocardial perfusion scintigraphy was also performed. At angiography, 30 patients (Group A), had more severe disease (Gensini score: 46.9 +/- 16) and angiographically visible collaterals (grade 2-3 Cohen and Rentrop classification) perfusing the ischaemic zone; the other 30 (Group B), had lesser disease (Gensini score: 28.6 +/- 18, p less than 0.001 vs Group A) and non visible collaterals to the ischaemic areas. Maximal ST depression and total exercise duration were similar in the 2 groups (2.5 +/- 0.6 vs 2.5 +/- 0.7 mV and 6.2 +/- 1.8 vs 6.8 +/- 1.9 min, respectively) but time and rate-pressure product to 1 mm ST depression were lesser in Group A (3.5 +/- 0.8 vs 4.8 +/- 0.6 min, p less than 0.01, and 14189 +/- 2451 vs 16081 +/- 2215 b/min x mmHg, p less than 0.04). Surprisingly, in Group A, the ST segment returned to the baseline more rapidly (5.5 +/- 1.6 vs 11.7 +/- 3.3 min, p less than 0.001), and the ischaemic area [time (s) x ST (mV)], measured in the recovery period, was also smaller (301 +/- 163 vs 621 +/- 260, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Intravenous nitroglycerin infusion suppresses exercise-induced arrhythmia in patients with ischemic cardiopathy: indications for chronic treatment ].

In patients with ischemic heart disease and arrhythmias, selection of antiarrhythmic treatment is often difficult as it is hard to separate "primary" from ischemic arrhythmias. We studied 20 patients with ischemic heart disease, who developed ventricular arrhythmias consistently during exercise test. Exercise test was performed twice during infusion of placebo and then during intravenous administration of nitroglycerin, titrated to reduce systolic blood pressure by 10 mmHg. Exercise duration was 7.8 +/- 1.7 and 7.9 +/- 1.5 min, in the 2 placebo tests (NS). Angina developed in 5 patients and ischemic ST changes in 10. With nitroglycerin exercise duration increased to 8.4 +/- 20 min (p less than 0.05), diagnostic ST segment depression was observed in 2 patients and only 1 had angina. In all 20 patients, ventricular arrhythmias were consistently present during both tests on placebo, that were markedly reduced by nitroglycerin. In fact, ventricular ectopic beats were 455 (mean 35.8 +/- 16.8) and 418 (mean 34.4 +/- 11.1) in the 2 exercise tests with placebo, and 11 during nitroglycerin infusion (mean 0.6 +/- 0.1; p less than 0.001). Couplets were 28 and 29 during placebo (NS) and 0 during nitroglycerin (p less than 0.001). Ventricular tachycardia was present in 6 and 8 patients during placebo but in none during nitroglycerin (p less than 0.001). Reduction of exercise-induced arrhythmias was maintained during chronic treatment with oral vasodilators. Prevention of exercise-related arrhythmias by nitroglycerin infusion appears a good indicator of their ischemic origin and may provide valuable information for long-term profilaxis with oral vasodilators, then avoiding the use of antiarrhythmic agents and their potential side effects.

Adult↗

[Left atrial enlargement during the exercise test: a new electrocardiographic sign of transitory ischemia].

In patients with coronary artery disease, electrocardiographic signs of left atrial enlargement (LAE-negative P wave deflection greater than or equal to 1 mm2 in lead V1) are associated with increased left ventricular end diastolic pressure (LVEDP). We investigated the possibility that transient LAE could represent an additional criterion for diagnosing myocardial ischemia during exercise testing (EST). We studied 48 consecutive patients with chronic stable angina, positive EST and 201 Tl scintigraphy, and angiographically proven CAD; 200 other consecutive patients with atypical chest pain and normal stress/rest 201 Tl scintigraphy served as controls. During EST, transient LAE developed in 34/48 patients with CAD but in only 1/200 controls (p less than 0.001). When present, LAE preceded ST changes (6.1 +/- 1 min vs 8.2 +/- 2 min) and recovered earlier (4.7 +/- 4 min vs 5.8 +/- 3 min). The prevalence of 2-3 vessel CAD was significantly higher in patients with EST-induced LAE (54% vs 34%, p less than 0.05). In conclusion, transient ECG signs of LAE during EST represent a highly specific sign of reversible ischemia and are frequently associated with multivessel CAD. Although less sensitive than classical ST criteria, this sign may prove useful in patients exhibiting equivocal ST changes and in the presence of ventricular conduction disturbances.

Aged↗

Limitations of dipyridamole-echocardiography in effort angina pectoris.

The sensitivity of dipyridamole--2-dimensional (2-D) echocardiography was assessed for detection and localization of ischemia in 21 patients with severe chronic stable angina pectoris, a clearly positive exercise stress test response and multivessel coronary atherosclerosis. Regional wall motion during dipyridamole infusion (0.6 mg/kg intravenously over 4 minutes) was compared with control and recovery by 2 blinded observers in consensus. Transient regional wall motion abnormalities were observed in 11 patients. Angina and ST-segment changes occurred in 9 of these 11 patients with positive responses, but in none of those who showed no transient abnormality of regional wall motion. Localization of regional wall motion abnormalities correlated well with angiographic severity of coronary lesions. Endocardial area contraction, evaluated by a computerized system, was reduced significantly after dipyridamole administration in patients with a positive response (from 51 +/- 10% to 35 +/- 11%, p less than 0.001), whereas it did not change significantly in the others (from 43 +/- 6% to 42 +/- 8%). In the 11 patients with a positive response, coronary reserve assessed by exercise testing (modified Bruce protocol) was more impaired than in those with a negative response (time to 1 mm of ST depression 177 +/- 148 seconds and 472 +/- 179 seconds, respectively, p less than 0.01). In patients with severe angina and multivessel coronary artery disease, dipyridamole--2-D echocardiography appears to identify the vessel in which flow reserve is most limited. Although this information may be valuable, indications for the test are restricted to patients with severely limited exercise capacity.

Adult↗