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Biomedical subjects

L Chiariello

Publications and source records attributed to L Chiariello.

At least 91 records · Page 5Linked to original sources
PubMed1994

Determinants of myocardial ischemia during percutaneous transluminal coronary angioplasty in patients with significant narrowing of a single coronary artery and stable or unstable angina pectoris.

Previous studies have assessed the determinants of collateral vessel recruitment during coronary occlusion in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). However, the determinants of severity of myocardial ischemia after sudden coronary occlusion do not necessarily coincide with those responsible for collateral vessel recruitment. The aim of this study was to assess the determinants of severity of myocardial ischemia during balloon inflation by recording surface and intra-coronary electrocardiograms (ECGs). In 62 consecutive patients with 1-vessel disease and without previous myocardial infarction undergoing successful PTCA for stable (n = 33) or unstable (n = 29) angina pectoris, the summation of the absolute values of ST-segment shifts from baseline on the intracoronary and surface ECG at the end of the first 2-minute inflation was obtained as an index of the severity of myocardial ischemia. Stenosis severity before PTCA was measured using computerized coronary angiography, while the grade of collateral filling was scored according to Rentrop's classification. The mean (+/- 1 SD) ST-segment shift at the end of balloon inflation was less in patients with than without collateral vessels (12 +/- 10 vs 23 +/- 15 mm, p < 0.05). Despite a similar prevalence of collateral vessels (34% vs 24%, p = NS), the mean ST-segment shift was also less in patients with unstable than stable angina (15 +/- 9 vs 24 +/- 17 mm, p < 0.05). However, the mean ST-segment shift was not associated with the severity of coronary stenosis before PTCA (r = 0.0004, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Substance P potentiates the algogenic effects of intraarterial infusion of adenosine.

OBJECTIVES: This study investigated whether substance P potentiates the muscular and cardiac pain caused by the intraarterial infusion of adenosine, an autocoid known to induce muscular and cardiac ischemic-like pain in humans. BACKGROUND: Substance P is involved in the generation of neurogenic inflammation and causes cutaneous hyperalgesia. Because substance P is present in perivascular nerves it might also cause muscular and cardiac hyperalgesia. To test this hypothesis its effects on adenosine-induced muscular and cardiac pain were investigated in humans. METHODS: A randomized, crossover study of the algogenic effects of the intrailiac infusion of increasing scalar doses (from 125 to 2,000 micrograms/min) of adenosine or substance P (11.2 pmol/min) for 3 min, followed by the simultaneous infusion of substance P plus the same doses of adenosine, was carried out in nine patients with no evidence of peripheral vascular disease. A similar protocol was carried out by infusing increasing scalar doses of adenosine (from 50 to 800 micrograms/min) or substance P (11.2 pmol/min) for 3 min, followed by the simultaneous infusion of substance P plus the same doses of adenosine, into the left coronary artery of eight patients with angina. Pain severity, assessed by a visual analog scale, is presented as median. The remaining data are presented as mean value +/- 1 SD. RESULTS: All patients experienced pain during both adenosine and substance P plus adenosine infusion; no patient experienced pain during the infusion of substance P alone. During intrailiac infusion, all patients experienced pain in the right leg that occurred earlier (207 +/- 152 vs. 321 +/- 154 s, p < 0.05) and was greater (47 vs. 30 mm, p < 0.05) during the simultaneous infusion of substance P plus adenosine than during the infusion of adenosine. Similarly, during intracoronary infusion, all patients experienced chest pain that occurred earlier (409 +/- 242 vs. 596 +/- 210 s, p < 0.05) and was greater (51 vs. 33 mm, p < 0.05) during the simultaneous infusion of substance P plus adenosine than during infusion of adenosine. No patient exhibited electrocardiographic signs of ischemia. CONCLUSIONS: Substance P does not cause muscular or cardiac pain, but it provokes muscular and cardiac hyperalgesia.

Adenosine↗
PubMed1994

Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K+ channel blocker.

BACKGROUND: Brief episodes of ischemia render the heart more resistant to subsequent ischemia; this phenomenon has been called ischemic preconditioning. In some animal species, myocardial preconditioning appears to be due to activation of ATP-sensitive K+ (KATP) channels. The role played by KATP channels in preconditioning in humans remains unknown. The aim of this study was to establish whether glibenclamide, a selective KATP channel blocker, abolishes the ischemic preconditioning observed in humans during coronary angioplasty following repeated balloon inflations. METHODS AND RESULTS: Twenty consecutive patients undergoing one-vessel coronary angioplasty were randomized to receive 10 mg oral glibenclamide or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 mL/min) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusion, both patient groups underwent coronary angioplasty. The mean values (+/- 1 SD) of ST-segment shifts on the surface 12-lead ECG and the intracoronary ECG were measured at the end of the first and second balloon inflations, both 2 minutes long. In glibenclamide-treated patients, the mean ST-segment shift during the second balloon inflation was similar to that observed during the first inflation (23 +/- 13 versus 20 +/- 8 mm, P = NS), and the severity of cardiac pain was greater (55 +/- 21 versus 43 +/- 23 mm on a scale of 0 to 100, P < .05). Conversely, in placebo-treated patients the mean ST-segment shift during the second inflation was less than that during the first inflation (9 +/- 5 versus 23 +/- 13 mm, P < .001), as was the severity of cardiac pain (15 +/- 15 versus 42 +/- 19 mm, P < .01). Blood glucose levels were significantly reduced 60 minutes after glibenclamide compared with those at baseline (53 +/- 9 versus 102 +/- 10 mg/100 mL, P < .001) in the glibenclamide group; however, before coronary angioplasty, blood glucose levels increased to 95 +/- 19 mg/100 mL, a value similar to that found in placebo group (96 +/- 11 mg/100 mL, P = NS). CONCLUSIONS: In humans, ischemic preconditioning during brief repeated coronary occlusions is completely abolished by pretreatment with glibenclamide, thus suggesting that it is mainly mediated by KATP channels.

Adenosine Triphosphate↗
PubMed1994

[Arrhythmic symptoms and events in patients wearing an implantable automatic defibrillator].

BACKGROUND: Although symptoms can be of some help in identifying the arrhythmia related to implantable cardioverter-defibrillator (ICD) discharge, symptomatic supraventricular arrhythmias and asymptomatic ventricular tachycardia have been reported. METHODS: In 18 survivors of cardiac arrest implanted with an ICD, the symptoms and intracardiac electrograms were systematically evaluated, in order to better define a relationship between some symptoms and supraventricular or ventricular tachyarrhythmias. RESULTS: A total number of 249 arrhythmic episodes were detected by the ICD during a mean follow-up of 378 +/- 107 days (range 137 to 642). Within this time, in 15 out of 18 patients (83%) at least one arrhythmic event alerting the device occurred, determining a therapeutic attempt in 13 patients. Only 49% of the episode stored by the ICD were symptomatic. Symptoms like palpitations, dizziness, "going under" lacked of predictability for ventricular tachycardia; in contrast, patients describing a "hot flush", alone or associated with palpitations, lightheadedness, dizziness most commonly recognized a ventricular tachyarrhythmias. This symptom had a good sensitivity (72%) and a high specificity (95%) in detecting a sustained ventricular tachycardia. CONCLUSIONS: Since in most cases symptoms are not a reliable criterion for validating ICD discharges stored electrograms during ICD activation need to be considered for analysis. However, the data of this study showed the importance of "hot flush" as a key symptom for recognizing the occurrence of a sustained ventricular tachyarrhythmia.

Adult↗
PubMed1994

Kinking of internal carotid artery: is it a risk factor for cerebro-vascular damage in patients undergoing cardiac surgery?

The incidence of carotid artery kinking is reported from 4% to 25% in different studies. During cardiopulmonary by-pass (CPB) in cardiac surgery the hemodynamic effects related to the kinking could produce hypoperfusion especially if associated with atherosclerotic lesions of the carotid arteries. We report our experience of 653 patients (538 males, 115 females, mean age 58.3 years) studied by coronaroangiography and internal carotid artery duplex scanning during the period January 1991-December 1992. Thirty-seven patients (22 males, 15 females, mean age 64.9 years), revealed anomalies of the internal carotid artery classificated as tortuosity (9 patients; 24.4%), and kinking (28 patients; 75.6%). All but 4 patients underwent cardiac surgery isolated or associated with carotid thrombo-endarterectomy (TEA) with Dacron patch arterioplasty. Three patients died (8.1%), one of them from cerebrovascular accident. He was a patient who had thromboembolism from the ascending aorta but without associated atherosclerotic lesions of carotid arteries. Asymptomatic isolated internal carotid artery kinking does not seem to be a risk factor for neurological complications during CPB. If carotid kinking is symptomatic and associated with atherosclerotic plaque producing internal carotid artery stenosis greater than 75%, we strongly suggest surgical treatment before cardiac operation.

Arteriosclerosis↗
PubMed1994

Partial reversal by exercise of protective effect in atrial fibrillation inducibility in patients with an accessory atrioventricular connection: comparison between flecainide and propafenone.

We have prospectively evaluated the reversibility of the protective effect of propafenone (P) and flecainide (F) on atrial fibrillation (AFib) inducibility in 31 patients with a symptomatic accessory atrioventricular connection during exercise. Each patient underwent repeated transesophageal stimulation and exercise testing after a drug-free week, or after a week of P (900 mg/daily), or F (300 mg/daily) given orally. The end point of the transesophageal stimulation was the induction of AFib. Because no AFib could be induced both at rest and at peak exercise, P or F was considered effective in 5 patients (16%) and 4 patients (13%), respectively. In contrast, drug therapy with P was totally ineffective in 10 patients (32%), while F was completely unable to control AFib induction in 14 patients (45%). A partial efficacy of antiarrhythmic drug therapy, in terms of AFib inducibility only at peak exercise, was achieved in 16 patients (52%) treated with P, and in 13 patients (40%) with F. The comparison of the mean R-R intervals during AFib between patients considered partial responders to drug therapy (AFib inducibility only at peak exercise) and those who completely failed any drug therapy did not show significant differences both at rest or during exercise. No correlation in the plasma concentration of P or F and AFib inducibility or duration was found. Thus, the data of this study shows that the reversible protective effect of IC antiarrhythmic class drugs by exercise seems related to inappropriate control on the substrate for AFib inducibility, and there exists a partially discrepant antiarrhythmic effect between the heart rate control during AFib and the inducibility of AFib.

Adult↗
PubMed1994

Doppler echocardiography evaluation of the CarboMedics valve in patients with small aortic anulus and valve prosthesis-body surface area mismatch.

A Doppler echocardiographic study was performed to evaluate the hemodynamic performances of small diameter CarboMedics aortic valves (CarboMedics, Inc., Austin, Tex.) in patients with a mismatch between the prosthetic valve and body surface area. Fourteen patients receiving either a 19 mm (n = 7) or a 21 mm valve (n = 7) prosthesis were studied. Only patients with a body surface area greater than 1.65 m2 were included in the study. Pulsed and continuous wave Doppler echocardiography was performed at rest and 2 minutes after treadmill exercise with the Bruce protocol. Peak and mean gradients across the valve prosthesis were estimated; effective orifice area, performance index, and discharge coefficient of the valve prosthesis were calculated. All patients achieved a significant increase in heart rate, systolic blood pressure, and cardiac output with exercise. Mean gradients +/- standard deviation of the mean at rest and 2 minutes after exercise were 20.1 +/- 7.1 mm Hg and 21.8 +/- 9 mm Hg for the 19 mm prosthesis and 12.3 +/- 3.4 mm Hg and 15.9 +/- 3.9 mm Hg for the 21 mm prosthesis. The 19 mm valve prosthesis significantly increased the effective orifice area with exercise (1.02 +/- 0.2 versus 1.20 +/- 0.3; p < 0.05), whereas it was almost unmodified for the 21 mm valve (1.38 +/- 0.2 versus 1.39 +/- 0.3; p = not significant). Therefore, despite a similar increase in cardiac output with exercise, only the 21 mm valve prosthesis showed a significant increase in peak (25.4 +/- 5.2 versus 34.9 +/- 8.1 mm Hg) and mean gradient (p < 0.01). We conclude that small diameter CarboMedics valves have satisfactory hemodynamic performances even after strenuous exercise in patients with large body surface areas. The hemodynamic performances of the 19 mm valve prosthesis seem to be optimized with exercise.

Aged↗
PubMed1993

Left ventricular volumes during exercise in normal subjects and patients with dilated cardiomyopathy assessed by first-pass radionuclide angiography.

During isotonic exercise, left ventricular (LV) suction and the Frank-Starling law of the heart may have important roles in the enhancement of early LV diastolic filling and in the increase of myocardial contractility, respectively. It remains controversial whether these mechanisms operate in normal subjects or patients with dilated cardiomyopathy. Ten healthy subjects and 10 patients with idiopathic dilated cardiomyopathy who underwent maximal upright bicycle exercise testing were studied. First-pass radionuclide angiography was performed at both rest and peak exercise using a multicrystal gamma camera. In normal subjects, LV end-systolic volume at peak exercise was smaller than during baseline (17 +/- 7 vs 30 +/- 15 ml/m2; p < 0.05), whereas rapid filling volume was greater (52 +/- 16 vs 38 +/- 8 ml/m2; p < 0.01). In patients with dilated cardiomyopathy, both end-systolic (108 +/- 34 to 123 +/- 53 ml/m2; p = NS) and rapid filling (24 +/- 6 to 28 +/- 9 ml/m2; p = NS) volumes did not change from rest to peak exercise. A significant correlation was found between the changes in end-systolic volume at peak exercise and in peak rapid filling rate in normal subjects (r = 0.6; p < 0.05), but not in patients with dilated cardiomyopathy (r = 0.3; p = NS). In normal subjects, end-diastolic volume at peak exercise was similar to that during baseline (78 +/- 14 and 85 +/- 15 ml/m2, respectively; p = NS), whereas in patients with dilated cardiomyopathy, it was greater (164 +/- 50 vs 146 +/- 33 ml/m2; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Right coronary artery cirsoid with fistulous connection to the coronary sinus.

A 61-yr-old woman was referred to our hospital for evaluation of a suspected right atrial myxoma. The transesophageal echocardiogram suggested the presence of an anomalous right coronary artery with fistulous connection to the coronary sinus. At cardiac catheterization, an oxygen step-up in the right atrium indicated a 1.3:1.0 left-to-right shunt. Aortic root angiography showed a large and calcified right coronary artery cirsoid draining to the coronary sinus, which appeared remarkably dilated. In this rare anomaly, cardiac catheterization is necessary, not only to quantify the magnitude of the left-to-right shunt, which is an important requirement for the indication to surgical treatment, but also to confirm the echocardiographic diagnosis.

Cardiac Catheterization↗
PubMed1993

Mechanisms of cardiac pain during coronary angioplasty.

OBJECTIVES: This study was conducted to establish whether the cardiac pain patients experience during coronary angioplasty is modulated by 1) the stretching of the coronary artery wall, and 2) the mechanisms responsible for the ischemic preconditioning. BACKGROUND: Anecdotal experimental observations indicate that stretching of the coronary artery wall is a stimulus adequate to cause cardiac pain. Furthermore, recent experimental studies indicate that adenosine, a mediator of the anginal pain, appears to play an important role in the genesis of ischemic preconditioning. METHODS: We randomly allocated 48 consecutive patients undergoing coronary angioplasty into two groups. In Group A the second balloon inflation was performed at a higher level than the first; in Group B the first two inflations were performed at the same level of balloon pressure. The mean values (+/- 1 SD) of ST segment shift on the surface 12-lead electrocardiogram (ECG) and the intracoronary ECG were measured at the end of each inflation period. Severity of cardiac pain was also obtained at the same time by using a visual analog scale. RESULTS: The mean ST segment shift during the second balloon inflation was significantly less than that during the first inflation in both groups of patients (12.8 +/- 9.3 vs. 18.5 +/- 11.9 mm, p < 0.001 and 13.7 +/- 10.1 vs. 21.3 +/- 13.9 mm, p < 0.001, respectively, in Groups A and B). Yet, the severity of cardiac pain during the second inflation was greater than that during the first inflation in Group A (40.8 +/- 32.7 vs. 26.9 +/- 27.2 mm, p < 0.01), whereas it was lesser in Group B (23.1 +/- 20.7 vs. 32.9 +/- 29.6 mm, p < 0.05). However, in the latter group, pain severity after normalization for the mean ST segment shift was similar during the first and second inflations (2.1 +/- 2.4 vs. 2.7 +/- 3.6, p = NS). CONCLUSIONS: During coronary angioplasty, the cardiac pain experienced by patients is caused in part by stretching of the coronary artery wall. If the stretching is maintained at a constant level during repeated coronary occlusions, the cardiac pain is entirely predicted by the severity of myocardial ischemia and therefore does not appear to be directly modulated by the mechanisms responsible for the ischemic preconditioning.

Adenosine↗
PubMed1993

Improvement of cardiac function in patients with severe congestive heart failure and coronary artery disease by dual chamber pacing with shortened AV delay.

Medical therapy often fails to control symptoms of severe heart failure. The possibility of modifying to some degree the global ventricular performance with the implantation of a physiological dual chamber pacemaker, set with a short atrioventricular delay (100 msec), has been adopted in two patients with severe heart failure due to coronary artery disease. The baseline clinical condition of both patients was characterized by leg edema, ascites, dyspnea at rest, or even orthopnea with a functional New York Heart Association (NYHA) class III-IV. Acute measurements of hemodynamic and echocardiographic parameters during stepwise shortening of AV interval guided the pacemaker implantation and setting of AV delay in the chronic phase. Within a few days after pacemaker implantation, both patients considerably improved their clinical status as well as their functional NYHA class, improving to class II in one patient and to class II-III in the other patient. In addition, modification of systolic and diastolic parameters paralleled these improvements functional class and clinical condition. Pacemaker therapy in severe heart failure refractory to medical therapy can be of considerable benefit in patients whose quality-of-life is severely compromised when pharmacological therapy is no longer effective. Acute hemodynamic and echocardiographic testing is useful in assessing the most appropriate AV delay and pacing mode.

Aged↗
PubMed1993

Bamiphylline improves exercise-induced myocardial ischemia through a novel mechanism of action.

BACKGROUND: In patients with stable angina pectoris aminophylline, a nonselective antagonist of adenosine receptors, markedly improves exercise capacity. To establish the role played by A1 adenosine receptors in the anti-ischemic action of aminophylline, the effects of bamiphylline, a selective A1 antagonist, on exercise-induced ischemia were investigated in patients with stable angina pectoris. METHODS AND RESULTS: In a single-blind, placebo-controlled, randomized cross-over trial in 18 patients, oral administration of 1200 mg bamiphylline increased both the time to 1-mm ST segment depression (from 524 +/- 177 to 664 +/- 192 seconds, P < .01) and the rate-pressure product at 1-mm ST segment depression (from 159 +/- 31 to 190 +/- 34 beats per minute per mm Hg/10(2) (P < .001). End-diastolic and end-systolic left ventricular volumes, left ventricular ejection fraction, and systolic septal and posterior wall thickening investigated by two-dimensional echocardiography in 12 of the 18 patients were not affected by oral administration of bamiphylline (124 +/- 22 versus 125 +/- 20 mL, P = NS; 49 +/- 12 versus 50 +/- 13 mL, P = NS; 60 +/- 8% versus 58 +/- 7%, P = NS; 35 +/- 6% versus 36 +/- 7%, P = NS; 32 +/- 6% versus 33 +/- 6%, P = NS, respectively). In 7 of the 18 patients, the intravenous infusion of bamiphylline (5 mg/kg in 15 minutes) during cardiac catheterization did not produce any significant change of heart rate (76 +/- 10 versus 75 +/- 13 beats per minute, P = NS), mean right atrial pressure (3.8 +/- 1.7 versus 3.7 +/- 1.7 mm Hg, P = NS), mean aortic pressure (102 +/- 12 versus 99 +/- 10 mm Hg, P = NS), or left ventricular end-diastolic pressure (14 +/- 3 versus 14 +/- 4 mm Hg, P = NS) compared with baseline. Furthermore, after intravenous infusion of bamiphylline, the diameter of seven proximal and distal normal segments and of seven stenotic segments were similar to those measured at baseline (3.1 +/- 0.5 versus 3.1 +/- 0.5 mm, P = NS; 1.6 +/- 0.2 versus 1.7 +/- 0.2 mm, P = NS; 1.6 +/- 0.5 versus 1.6 +/- 0.5 mm, P = NS, respectively). CONCLUSIONS: In patients with stable angina pectoris, oral administration of bamiphylline improves exercise capacity. Its anti-ischemic action does not appear to be mediated by systemic hemodynamic effects or by stenosis dilation. Therefore, the improvement of myocardial ischemia caused by bamiphylline is probably due to redistribution of coronary blood flow toward the underperfused subendocardium. This novel anti-ischemic action would appear to be mediated by antagonism of A1 receptors.

Aged↗
PubMed1993

[Unstable angina: the point of view of the surgeon].

Unstable angina is a serious condition with high risk of early coronary events; coronary revascularization in these patients gives good results but carries higher operative risk than in stable angina patients. Full medical therapy with antiischemic agents may be effective in controlling symptoms and preventing death and is therefore the first treatment of choice; as in stable angina, further treatment is indicated in stabilized patients according to non invasive tests results and coronary angiograms. Non responsive unstable patients have a poor outcome and are candidates for revascularization: angioplasty may be preferred in single or double vessel disease and bypass operation in multivessel disease. However, surgical revascularization in single and double vessel disease with critical proximal stenosis of a large anterior descending gives optimal results in our experience and may be the treatment of choice also in these patients. Because of the higher operative risk in multivessel disease in unstable ischemia, a combined procedure with angioplasty of the "culprit" lesion followed by full revascularization at a later time may be a more favourable option in some patients with multivessel disease.

Aged↗
PubMed1992

Prolonged asymptomatic catheter-induced left and right coronary artery spasm resistant to high dose of intracoronary nitroglycerin.

A 58-year-old woman, referred to our hospital to undergo invasive assessment of mitral valve stenosis, demonstrated prolonged asymptomatic catheter-induced left anterior descending and right coronary artery spasm during coronary arteriography. Coronary spasms were not associated with ECG and arterial blood pressure changes. Intracoronary injection of nitroglycerin (300 and 600 micrograms bolus) did not resolve coronary spasm. Coronary angiography, repeated 24 hours later using the same procedure and materials, did not show any evidence of coronary artery spasm. The present clinical case is interesting for 3 reasons. First, the presence of prolonged proximal double-vessel coronary spasm not associated with symptoms or signs of acute myocardial ischemia; second, the incapacity of high dose of intracoronary nitroglycerin to resolve the coronary spasm; third, the dramatic changes in the sensitivity of coronary artery to mechanical stimulation in different days.

Cardiac Catheterization↗