[Diastolic filling and the law of Frank-Starling].
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Diastole↗
Biomedical subjects
F Tomai
Publications and source records attributed to F Tomai.
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↗
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↗
Risk factors in schoolchildren associated with a family history of unheralded myocardial infarction or uncomplicated stable angina in male relatives.
OBJECTIVES: The aim of this study was to compare risk factors for coronary atherosclerosis in children with a family history of unheralded myocardial infarction or uncomplicated stable angina. BACKGROUND: In patients with unheralded myocardial infarction, coronary atherosclerosis might have a greater tendency to cause acute coronary occlusion than in patients with uncomplicated stable angina, suggesting the possibility of different risk factors in these two groups of patients. METHODS: Serum lipid levels were compared in children with a family history of unheralded myocardial infarction (236 children) or uncomplicated stable angina (48 children) or no family history of ischemic heart disease (613 children). RESULTS: Mean (+/- 1 SD) total serum cholesterol was higher in children with a family history of myocardial infarction than in control subjects (161 +/- 28 vs. 154 +/- 25 mg%, p < 0.01). In children with a family history of stable angina, mean total serum cholesterol (159 +/- 25 mg%) was similar to that in children with family history of myocardial infarction. High density lipoprotein cholesterol and apolipoprotein A-I were higher in children with family history of stable angina than in children with family history of myocardial infarction and control subjects (69 +/- 18 vs. 61 +/- 13 and 60 +/- 13 mg%, p < 0.01; 143 +/- 23 vs. 130 +/- 18 and 129 +/- 18 mg%, p < 0.01, respectively). In children with a family history of myocardial infarction, the low density/high density lipoprotein cholesterol ratio was significantly higher than in control subjects (1.53 +/- 0.64 vs. 1.44 +/- 0.56, p < 0.05). Conversely, in children with a family history of stable angina, this ratio (1.24 +/- 0.51) was significantly lower (p < 0.05) than in control subjects. CONCLUSIONS: Risk factors for coronary athersclerosis in children with a family history of unheralded myocardial infarction are different from those in children with a family history of uncomplicated stable angina. Higher levels of apolipoprotein A-I early in life might reduce the risk of acute coronary syndromes.
Adult↗
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↗
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↗
Evidence of cardiac suction in the presence of high end-diastolic filling pressure: a case report.
Cardiac suction has been previously demonstrated in the normal heart and in cardiac diseases characterized by a normal or reduced end-diastolic ventricular pressure. We report a patient with tight mitral stenosis and severe tricuspid regurgitation who provides the evidence of cardiac suction, despite the presence of increased end-diastolic pressures. The negative diastolic pressures observed in our patient appear to be related to the preservation of a vigorous contraction of both ventricles resulting in small end-systolic volumes. In this setting the elastic potential energy stored in the myocardium during each vigorous contraction is released during diastole, thus creating a negative pressure which sucks blood into the ventricles.
Diastole↗
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↗
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↗
Single-day combined evaluation of regional myocardial perfusion and function at rest and peak exercise with 99mTc-MIBI in patients with coronary artery disease.
99mTc-labeled methoxy-isobutyl-isonitrile (MIBI) allows a simultaneous radionuclide assessment of regional heart function and perfusion. In this study the effectiveness of functional and perfusional images obtained with 99mTc-MIBI in the detection of coronary stenoses was compared with that of their combination. We studied 197 patients who underwent coronary angiography and a single-day radionuclide protocol including first pass angiography (multicrystal gamma camera) and single photon emission computed tomography, by means of 2 injections of 99mTc-MIBI at rest and at peak exercise. Fifteen patients had < 50% stenoses, 50 had 1-vessel, 69 2-vessel and 63 3-vessel disease, for a total of 377 pathological major coronary vessels; 129 patients had previous myocardial infarction. Functional images, perfusional tomograms and their combination showed the same sensitivity (98%) and specificity (80%) in detecting coronary patients. Regional sensitivity and specificity of the combined analysis achieved 87% and 82%, respectively, vs. 94% (p < 0.005) and 60% (p < 0.001) of functional images, and 88% (p = N.S.) and 74% (p < 0.05) of perfusional tomograms. Thus, the combined analysis of regional functional and perfusional abnormalities increased significantly the specificity in the detection of coronary stenoses, in comparison with the separate evaluation of function and perfusion, achieving also a slightly higher diagnostic accuracy (85%, vs. 81% and 83%, respectively). The results confirm that a single-day protocol simultaneously assessing regional myocardial function and perfusion with 99mTc-MIBI represents a rapid and effective diagnostic method, that allows the physician to assess the presence and functional importance of coronary stenoses in less than 4 hours.
Coronary Disease↗
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↗
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↗
Peak exercise left ventricular performance in normal subjects and in athletes assessed by first-pass radionuclide angiography.
The role of Frank-Starling law of the heart in determining the increase in cardiac output during exercise in humans is still controversial (e.g., the mechanisms responsible for the enhancement of left ventricular [LV] filling during the shortened diastolic interval). Ten weight lifters, 12 swimmers and 12 sedentary subjects who underwent maximal upright bicycle exercise testing were studied. First-pass radionuclide angiography was performed both at rest and at peak exercise using a multicrystal gamma camera. Compared with resting values, heart rate and cardiac index at peak exercise increased by 101 +/- 16 beats/min (p less than 0.001) and 6.7 +/- 2.8 liters/min/m2 (p less than 0.001) in weight lifters, by 96 +/- 9 beats/min (p less than 0.001) and 9.5 +/- 2 liters/min/m2 (p less than 0.001) in swimmers, and by 103 +/- 9 beats/min (p less than 0.001) and 7.3 +/- 1.8 liters/min/m2 (p less than 0.001) in sedentary subjects. Stroke volume increased by 20.5 +/- 9.8 ml/m2 (p less than 0.001) in swimmers only. End-diastolic volume at peak exercise did not change in weight lifters and in swimmers; it decreased by 8.2 +/- 8.6 ml/m2 (p less than 0.01) in sedentary subjects. A significant correlation was found between the decrease in end-systolic volume and the increase in peak rapid filling rate at peak exercise in all 3 groups (r = 0.65, p less than 0.05 in weight lifters; r = 0.59, p less than 0.05 in swimmers; r = 0.67, p less than 0.05 in sedentary subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
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↗
Angiographic evidence of cardiac ventricular diastolic suction.
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Angiography↗
[Venous diseases of the lower limbs and pulmonary embolism].
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Adult↗
[Prognostic significance of acute nitrate administration in the preoperative evaluation of patients with post-infarct left ventricular aneurysm].
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Adult↗
[Clinico-hemodynamic evaluation of endomyocardial fibrosis. Description of a case].
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Adult↗