Effects of converting enzyme inhibition on baroreflex sensitivity in patients with myocardial infarction.

BACKGROUND: Baroreflex sensitivity provides useful prognostic information in patients after acute myocardial infarction. However, no data are available about the effects of converting enzyme inhibition on this variable. OBJECTIVES: The aim of the study was to evaluate the effects of angiotensin-converting enzyme inhibition on baroreflex sensitivity in patients after uncomplicated myocardial infarction. METHODS: Twenty-five patients after uncomplicated myocardial infarction underwent baroreflex sensitivity evaluation 72 to 96 h after symptom onset and after 4 days of captopril therapy. Twenty additional patients with the same characteristics were evaluated at the same time intervals before and after placebo administration to identify spontaneous baroreflex sensitivity variations. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in the RR interval. RESULTS: The mean baroreflex sensitivity value increased after captopril administration from 6.5 +/- 4.2 to 11.8 +/- 6.1 ms/mm Hg (p less than 0.01) and in individual analyses increased by greater than 2 ms/mm Hg in 68% of patients. Mean plasma renin activity increased after captopril from 3.7 +/- 2.4 to 8.5 +/- 4.9 ng/ml per h (p less than 0.005). No difference was detectable in baroreflex sensitivity and plasma renin activity values according to the site of necrosis. In the control group, baroreflex sensitivity and plasma renin activity remained unchanged between the two studies. CONCLUSIONS: This study demonstrates that in patients with uncomplicated myocardial infarction, captopril significantly improves the chronotropic response to baroreceptor stimulation.

Effects of late administration of tissue-type plasminogen activator on left ventricular remodeling and function after myocardial infarction.

To evaluate the effects of late thrombolysis on left ventricular volume and function in acute myocardial infarction, two-dimensional echocardiography and radionuclide angiography were performed before discharge and after 1 year of follow-up study in 34 patients with acute anterior myocardial infarction. Of these, 10 admitted to the coronary care unit within 4 h from the onset of symptoms were treated with recombinant tissue-type plasminogen activator (rt-PA) (Group A) and 24 admitted between 4 and 8 h after onset were randomly assigned to receive either rt-PA (Group B, n = 12) or conventional therapy (Group C, n = 12). Seven to 10 days after admission, all patients underwent cardiac catheterization and coronary angiography. Patency of the infarct-related vessel was 70% in Group A, 66% in Group B and 33% in Group C and the average Thrombolysis in Myocardial Infarction (TIMI) coronary perfusion grade was 1.9 +/- 0.8 for Group A, 1.6 +/- 1.0 for Group B and 0.84 +/- 0.95 for Group C (Group A versus Group C p less than 0.01; Group B versus Group C p less than 0.05). At predischarge evaluation, mean left ventricular end-systolic and end-diastolic volumes were higher in Group C than in Group B (p less than 0.001 and 0.05, respectively) and Group A (p less than 0.005 for both); mean left ventricular ejection fraction at rest was lower in Group C than in Group B and Group A (p less than 0.05 for both). At 1 year follow-up study, end-systolic and end-diastolic volumes remained higher in Group C than in Group B (p less than 0.05 for both) and Group A (p less than 0.005 for end-systolic volume and p less than 0.001 for end-diastolic volume); ejection fraction at rest was lower in Group C than in Groups A and B (p less than 0.05 for both); during exercise, it increased more in Group A than in Group C (p less than 0.01). Comparison of data obtained before discharge and at the 1 year follow-up study revealed a significant differences in end-systolic volume (p less than 0.05) in Group C patients and in end-diastolic volume in patients in Groups B (p less than 0.05) and C (p less than 0.001). The beneficial effect of late thrombolysis with rt-PA may be related to a reduction in myocardial expansion and thus to a favorable influence on postinfarction left ventricular remodeling.

Effects of captopril treatment on left ventricular remodeling and function after anterior myocardial infarction: comparison with digitalis.

The effects of captopril and digoxin treatment on left ventricular remodeling and function after anterior myocardial infarction were evaluated in a randomized unblinded trial. Fifty-two patients with a first transmural anterior myocardial infarction and a radionuclide left ventricular ejection fraction less than 40% were randomly assigned to treatment with captopril (Group A) or digoxin (Group B). The two groups had similar baseline hemodynamic, coronary angiographic, echocardiographic and radionuclide angiographic variables. Among the 40 patients (20 in each group) who were followed up for 1 year, echocardiographic end-diastolic and end-systolic volumes were unmodified in Group A and global wall motion index was improved (p less than 0.01); in Group B, end-diastolic and end-systolic volumes increased (p less than 0.001 for both) and global wall motion index was unchanged. Rest radionuclide ejection fraction increased significantly in both groups (p less than 0.001, Group A; p less than 0.005, Group B). A comparison of the changes in the considered variables between the two groups after 1 year of treatment showed a difference in end-diastolic (p less than 0.005) end-systolic volumes (p less than 0.001) and global wall motion index (p less than 0.005) without differences in radionuclide ejection fraction, which improved to a similar degree in both groups. The results of this study suggest that captopril therapy, started 7 to 10 days after symptom onset in patients with anterior myocardial infarction and an ejection fraction less than 40%, improves both left ventricular remodeling and function and prevents left ventricular enlargement and in these patients performs better than digitalis.

Influence of reversible segmental left ventricular dysfunction on heart period variability in patients with one-vessel coronary artery disease.

OBJECTIVES: This study evaluated the relation between reversible segmental left ventricular dysfunction and frequency domain measures of heart period variability in patients with coronary artery disease. BACKGROUND: Heart period variability is frequently reduced in patients with coronary artery disease. However, the mechanisms of this reduction are still unclear. METHODS: Echocardiographic left ventricular wall motion and frequency domain measures of heart period variability were evaluated in 32 patients with one-vessel coronary artery disease before and 16 to 24 days after successful percutaneous transluminal coronary angioplasty. Of these, 12 patients (Group A) had normal and 20 patients (Group B) had abnormal regional wall motion. A control group of 15 healthy subjects (Group C) underwent 24-h Holter recording twice at 2-week intervals to check for spontaneous variations. RESULTS: At baseline, low and high frequency power were lower in Group B than in Groups A and C, whereas no difference was detectable in ultra low and very low frequency and total power. After coronary angioplasty, regional wall motion and frequency domain measures of heart period variability were unchanged in Group A. In Group B the mean (+/- SD) summed segment score improved from 17.1 +/- 3.6 to 12.8 +/- 2.0 (p < 0.01), and mean low and high frequency power (logarithmic units) increased from 6.14 +/- 0.23 to 6.35 +/- 0.34 (p < 0.01) and from 5.43 +/- 0.32 to 5.68 +/- 0.52 (p < 0.01), respectively. Furthermore, low and high frequency power, lower at baseline in Group B than in the other two groups, were comparable in the three groups after coronary angioplasty. CONCLUSIONS: This study demonstrates that segmental left ventricular dysfunction is involved in determining sympathovagal imbalance in patients with one-vessel coronary artery disease; the reversal of left ventricular dysfunction by successful coronary angioplasty improves the heart period power spectrum. Thus, alterations in cardiac geometry influence the discharge of afferent sympathetic mechanoreceptors, contributing to the derangement in autonomic control of heart rate.

Role of increased cholinergic activity in reperfusion induced ventricular arrhythmias.

The effect of increased cholinergic activity on reperfusion induced ventricular arrhythmias was studied in alpha chloralose anaesthetised dogs by administering neostigmine during a 25 min occlusion of the anterior left descending coronary artery. The dogs were divided into five groups, each of 10 animals: the control group received only saline solution; group 1 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion (that is, 5 min before reperfusion); group 2 atropine 0.4 mg.kg-1 iv at 10 min of coronary occlusion and neostigmine 0.03 mg.kg-1 iv at 20 min; and group 3 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion and at the same time underwent atrial pacing at the same rate as that of the sinus node just before neostigmine administration. In group 4 heart rate was slowed (junctional rhythm) by destroying the sinus node at 20 min of coronary occlusion. The results obtained showed that ventricular tachycardia and fibrillation, which occur at the beginning of reperfusion, were significantly less frequent in group 1 (p less than 0.001) and in group 4 (p less than 0.001). The protective action of neostigmine was abolished by previous administration of atropine (group 2) and modified by preventing the decrease in the heart rate by atrial pacing (group 3). In group 3 ventricular tachycardia was more frequent but the incidence of ventricular fibrillation was reduced significantly compared with the control and atropine groups. Thus cholinergic activity has a protective role in reperfusion arrhythmias by decreasing the heart rate before release of the coronary occlusion and therefore reduces the incidence of ventricular fibrillation.

Cardiovascular effects of depot long-acting somatostatin analog Sandostatin LAR in acromegaly.

Cardiovascular disease is the most severe complication of acromegaly accounting for the increased mortality of these patients. Recently, the slow-release form of octreotide (OCT; Sandostatin LAR, OCT-LAR), for im injection every 28 days, was reported to induce suppression of GH levels below 7.5 mU/L (2.5 microg/L) in 39-75% of patients, and normalization of insulin-like growth factor (IGF)-I levels for age in 64-88% of patients, with an excellent patients' compliance. The aim of the present study was to investigate the early effect of OCT-LAR treatment on the left ventricular (LV) structure and performance in 15 somatostatin analog-naive patients with acromegaly (GH, 94.8 +/- 24.9 mU/L; IGF-I, 757.9 +/- 66.6 microg/L), focusing on the early effect of GH and IGF-I suppression on the heart. Cardiac structure was investigated by echocardiography, whereas LV performance was investigated by gated-blood-pool scintigraphy, before and after 3 and 6 months of treatment with OCT-LAR. OCT-LAR was initially administered im, at a dose of 20 mg every 28 days, for 3 months. In six patients, the dose was then increased to 30 mg every 28 days to achieve disease control, which was considered when fasting and/or glucose-suppressed GH values were below 7.5 and 3.0 mU/L, respectively, together with IGF-I values within the normal range for age. The treatment with OCT-LAR for 6 months induced a significant decrease of GH (to 12.9 +/- 3.0 mU/L) and IGF-I levels (to 340.3 +/- 40.2 microg/L) in all 15 patients. After 6 months of treatment, the percent IGF-I suppression was 52.8 +/- 4.4%, and serum GH/IGF-I levels were normalized in 9 patients. A significant decrease of LV mass index (LVMi), interventricular septum thickness, and LV posterior wall thickness was observed in all 15 patients after 3 and 6 months of OCT-LAR treatment: LVMi was decreased by 19.1 +/- 2.0% without any difference in patients with (19.9 +/- 2.7%) or without disease control (17.8 +/- 3.3%). Among the 11 patients with LV hypertrophy, 6 normalized their LVMi after treatment. At study entry, an inadequate LV ejection fraction (LVEF) at rest (<50%) was found in 5 patients (33.3%), whereas an impaired response of LVEF at peak exercise (<5% increase of basal value) was found in 9 patients (60%). A significant increase in LVEF, both at rest (from 51.6 +/- 2.6 to 58.1 +/- 1.7%, P < 0.01) and at peak exercise (from 51.6 +/- 2.3 to 60.2 +/- 2.4%, P < 0.001) was found in patients with (as compared with those without) disease control (from 55.2 +/- 3.8 to 58.0 +/- 4% and from 61.8 +/- 4.6 to 61.8 +/- 3.4%, respectively). Among the 5 patients with inadequate LVEF at rest, all but 1 regained a normal LVEF after 6 months of treatment; whereas, among the 9 patients with an impaired response of the LVEF at peak exercise, 3 patients normalized, 4 improved, and 2 impaired their responses after treatment. The percent of IGF-I suppression was significantly correlated with the percent increase of resting LVEF (r = 0.644, P < 0.01). Exercise duration (from 6.0 +/- 0.7 to 7.3 +/- 0.7 min) and capacity (from 69.0 +/- 8.2 to 80 +/- 7.8 watts) were increased in the 15 patients considered as a whole, but the improvement in the exercise response was significant only in patients with disease control (P < 0.01 and P < 0.05, respectively) who also had an increase in the peak ejection rate (P = 0.03). No change in hemodynamic parameters, either at rest or at peak exercise, was found after treatment with OCT-LAR in the 15 patients. In conclusion, the results of the present study demonstrate that OCT-LAR im injections every 28 days induces a sustained suppression of GH levels and IGF-I levels in all acromegalic patients, allowing achievement of disease control in 60% of patients after 6 months of treatment. The sustained suppression of IGF-I levels was followed by a significant reduction of LVMi in all patients already after 3 months of treatment, with recovery of LV hypertrophy in 6 of 11 patients. (ABSTRACT TRUN

Effect of 1 year of lisinopril treatment on cardiac autonomic control in hypertensive patients with left ventricular hypertrophy.

In this study we evaluated in hypertensive patients the effects of drug-induced left ventricular hypertrophy regression on cardiac autonomic control, as assessed by means of heart period variability analysis. Power spectral analysis of 24-hour electrocardiographic monitoring was performed in 30 hypertensive patients with left ventricular hypertrophy at baseline, after 1 year of lisinopril treatment, and after 1 month of drug withdrawal. At the same times, patients underwent 24-hour blood pressure monitoring, echocardiographic study, and plasma renin activity assessment. Lisinopril treatment increased plasma renin activity and reduced 24-hour systolic and diastolic pressures (from 159 +/- 14 to 121 +/- 8 and from 103 +/- 7 to 80 +/- 3 mm Hg, respectively) and left ventricular mass index (from 159 +/- 33 to 134 +/- 26 g/m2); moreover, in 12 of 30 patients, left ventricular mass normalization was achieved. Drug withdrawal was followed by an increase in blood pressure without left ventricular mass modification. In the total study population, only high-frequency power was higher after lisinopril treatment. In the subgroup of patients with left ventricular mass normalization, daytime and nighttime high-frequency powers as well as nighttime total and very-low-frequency powers were higher after 1 year of treatment than at baseline. In the remaining 18 patients, power spectral measures after treatment were slightly lower than at baseline and were even lower after drug withdrawal. Thus, in hypertensive hypertrophic patients, lisinopril treatment improves sympathovagal imbalance when left ventricular mass normalization is achieved. In patients without left ventricular mass normalization, drug withdrawal is followed by a worsening of neural cardiac control.

Improved cardiovascular risk factors and cardiac performance after 12 months of growth hormone (GH) replacement in young adult patients with GH deficiency.

Adult GH deficiency (GHD) is associated with increased cardiovascular morbidity and mortality due to unfavorable lipid profile, hyperfibrinogenemia, and impairment of cardiac performance. This prospective controlled cohort study evaluated the effects of 12-month GH replacement on lipid profile, fibrinogen levels, cardiac mass by echocardiography, and performance by equilibrium radionuclide angiography. To this end we studied 20 patients (11 men and 9 women, aged 19-40 yr), 10 with childhood-onset (co-) and 10 with adult-onset (ao-) disease, and 20 sex- and age-matched healthy subjects. At study entry, insulin-like growth factor I (IGF-I; P < 0.0001) and high density lipoprotein (HDL) cholesterol (P < 0.0001) levels, left ventricular mass index (LVMi; P < 0.0001), ejection fraction (LVEF) at rest (P = 0.001) and at peak exercise (P < 0.0001), peak ejection rate (P = 0.005), and exercise duration (P < 0.0001) and capacity (P = 0.002) were lower, whereas total cholesterol (P = 0.02), triglycerides (P = 0.003), and fibrinogen (P = 0.005) levels were higher in patients than in controls. After 12 months, increases in IGF-I (P < 0.0001) and HDL cholesterol levels (P = 0.04), LVMi (P < 0.0001), LVEF at peak exercise (P < 0.0001), and exercise duration (P = 0.009) and capacity (P = 0.003) and decreases in total cholesterol (P < 0.0001), low density lipoprotein cholesterol (P < 0.0001), triglycerides (P < 0.0001), and fibrinogen (P = 0.01) levels were found in all patients, without any difference between co- and ao-GHD. At the end of treatment, however, total cholesterol, triglycerides, and fibrinogen levels were still higher, and HDL cholesterol levels, IGF-I levels, and LVEF at rest and at peak exercise were lower in patients than in controls. In conclusion, GH replacement for 12 months significantly improved lipid profile, decreased fibrinogen levels, and increased LVMi and LVEF in young adults with co- or ao-GHD. However, lipid profile, fibrinogen levels, and systolic function remained abnormal compared with those in age- and sex-matched controls, suggesting that a longer period of GH replacement is necessary to normalize cardiovascular parameters and reverse the cardiovascular risk of these patients.

A multicenter, randomized double-blind study of valsartan/hydrochlorothiazide combination versus amlodipine in patients with mild to moderate hypertension.

OBJECTIVE: To compare the antihypertensive efficacy and tolerability of a once-daily fixed valsartan/hydrochlorothiazide (HCTZ) combination and amlodipine in subjects with mild-to-moderate hypertension. SUBJECTS AND SETTING: In this multicentre, double-blind, randomized, comparative trial, 690 patients with sitting systolic blood pressure (BP) > or = 160 mmHg and sitting diastolic BP > or = 95 mmHg at the end of a 2-week placebo wash-out period were randomized to valsartan-based treatment (n = 342) or amlodipine (n = 348). METHODS: The patients received valsartan 80 mg o.d. or amlodipine 5 mg o.d for 4 weeks; in the case of an unsatisfactory blood pressure response, the treatments could be respectively changed to the fixed combination of valsartan 80 mg + HCTZ 12.5 mg o.d. or amlodipine 10 mg o.d. for a further 8 weeks. RESULTS: Both treatment approaches decreased systolic blood pressure and diastolic blood pressure to the same extent. The rate of responders to treatment at the end of fourth week (before up-titration) was 57.4% among the valsartan-treated patients and 61.9% among the amlodipine-treated patients (ns). At the end of the study, the rate of responders was not significantly different between the two groups (74.9 versus 72.1%). Valsartan-based treatment had a slightly lower incidence of adverse events (1.5 versus 5.5%; P = 0.006). CONCLUSIONS: The results of this trial demonstrate that the valsartan/hydrochlorothiazide combination and amlodipine are equally effective in lowering BP, and that the combination is better tolerated.

Influence of left ventricular hypertrophy on heart period variability in patients with essential hypertension.

OBJECTIVE: To evaluate whether left ventricular hypertrophy in hypertensive patients is associated with a greater impairment of sympathovagal balance assessed by means of heart period variability. DESIGN AND METHODS: Forty hypertensive patients, 20 with echocardiographic evidence of left ventricular hypertrophy and 20 without, and 20 control subjects, were subjected to 24 h blood pressure monitoring and Holter recording on 2 consecutive days. Power spectrum analyses of heart period variability were performed utilizing the fast Fourier transform algorithm. RESULTS: No difference was detectable in 24 h, daytime and night-time blood pressure values between hypertensive patients with and without left ventricular hypertrophy. Low- and high-frequency powers were higher in controls than in hypertensives; in particular, low-frequency power showed a progressive decrease through control subjects and hypertensives without and with left ventricular hypertrophy. Furthermore, significant negative correlations were found between left ventricular mass index and low- and high-frequency power. No difference was detectable in ultra-low- and very low-frequency power. During daytime low- and high-frequency power were higher in controls than in hypertensives; during night-time, low- and high-frequency power increased significantly in all groups and low-frequency power was still higher in control subjects. CONCLUSIONS: Considering that, when analysed over 24 h Holter recording, low- and high-frequency power both reflected the parasympathetic modulation of heart rate, the present results demonstrate a parasympathetic withdrawal in hypertension; this sympathovagal imbalance is greater in patients with cardiac hypertrophy and is related to the increase in left ventricular mass.

Comparison of verapamil versus felodipine on heart rate variability in hypertensive patients.

OBJECTIVE: We evaluated the effect of two calcium channel blockers, verapamil and felodipine, on heart rate variability in hypertensive patients. DESIGN: Time and frequency domain measures of heart rate variability were obtained from 24 h Holter recording in 25 previously untreated hypertensive patients without left ventricular hypertrophy, before and after 3 months of verapamil slow-release treatment (240 mg once daily) or felodipine extended-release treatment (10 mg once daily). RESULTS: Blood pressure values decreased with both drugs. Measures of heart rate variability, comparable at baseline in the two groups, were unchanged after felodipine. After verapamil, the average RR interval, the square root of the mean of the squared differences between all adjacent normal RR intervals (r-MSSD) and the percentage of differences between all adjacent normal RR intervals > 50 ms (pNN50), measures of vagal modulation of heart rate, increased (from 735 +/- 67 to 827 +/- 84 ms, P < 0.001; from 30 +/- 10 to 44 +/- 15 ms, P < 0.001; and from 3 +/- 2 to 7 +/- 6%, P < 0.01, respectively) and were higher than after felodipine. The coefficient of variation, a measure that compensates for heart rate effects, increased only after verapamil (from 5.8 +/- 1.3% to 6.6 +/- 1.0%; P < 0.05). High frequency power and its coefficient of component variance, both representing the vagal modulation of heart rate, increased after verapamil (from 5.33 +/- 0.29 to 5.80 +/- 0.27 In units, P < 0.001 and from 1.9 +/- 0.3 to 2.2 +/- 0.25%; P < 0.05). Finally, the low to high frequency power ratio, an indicator of sympathovagal balance, with a high value suggesting a sympathetic predominance, decreased after verapamil (from 2.16 +/- 0.41 to 1.36 +/- 0.35; P < 0.001), confirming the improvement in vagal modulation of heart rate. CONCLUSION: In hypertensive patients, despite a comparable anti-hypertensive effect, verapamil, but not felodipine, has favourable effect on cardiac autonomic control.

Diastolic function in acute myocardial infarction: a radionuclide study.

We studied left ventricular diastolic function by equilibrium gated radionuclide angiography in patients as follows: 75 with acute myocardial infarction (AMI), 35 with anterior or anteroseptal necrosis (Group A) and 40 with inferior, inferolateral, or posterior necrosis (Group I). The ejection fraction (EF) was lower in Group A than Group I (41.9 +/- 2.5 vs. 57.1 +/- 2.0%, p less than 0.001), as was peak diastolic filling rate normalized to end diastolic volume (PDFR-EDV/sec) (1.9 +/- 0.1 vs. 2.4 +/- 0.1 EDV/sec, p less than 0.05). PDFR normalized to stroke volume was similar in both groups. An excellent linear correlation was found between EF and PDFR-EDV/sec in the total study population. Isovolumic relaxation period (IRP) was beyond our upper normal value of 94 msec in 64% of patients and it was shorter in Group A than I (95.8 +/- 12.7 vs. 147.0 +/- 13.6 msec, p less than 0.05). The presence of shorter IRP in Group A than in I is probably a result of an earlier mitral valve opening as a consequence of higher left atrial pressure.

Prediction of recovery of left ventricular dysfunction after acute myocardial infarction: comparison between 99mTc-sestamibi cardiac tomography and low-dose dobutamine echocardiography.

UNLABELLED: The aim of this study was to evaluate the role of 99mTc-sestamibi cardiac imaging and dobutamine echocardiography in detecting myocardial viability early after acute myocardial infarction. METHODS: Forty-nine patients (mean age 52 +/- 10 y) underwent coronary angiography, low-dose dobutamine echocardiography, radionuclide angiography and rest 99mTc-sestamibi imaging within 10 d after myocardial infarction. Of these patients, 19 were revascularized and 30 were treated medically. Resting echocardiogram and radionuclide angiography were repeated 8 mo later to evaluate segmental functional recovery and changes in left ventricular (LV) ejection fraction, respectively. RESULTS: In revascularized patients, 61 of 108 akinetic or dyskinetic segments showed functional recovery. In these patients, sensitivity in predicting segmental functional recovery was 87% for sestamibi imaging and 66% for dobutamine echocardiography (P < 0.001), whereas specificity and accuracy were comparable. Sestamibi activity (> or =55% of peak) was the strongest predictor of segmental functional recovery (P < 0.001) and of LV ejection fraction improvement > or =5% (P < 0.01) after revascularization. In medically treated patients, 60 of 149 akinetic or dyskinetic segments showed functional recovery. In these patients, the majority (94%) of segments with contractile reserve on dobutamine were viable on sestamibi imaging and 86% of them improved function at follow-up. Functional recovery was poor in segments without contractile reserve either with (38%) or without (62%) preserved sestamibi uptake. Inotropic response was the best predictor of segmental (P < 0.001) and global (P < 0.01) LV functional improvement in medically treated patients. CONCLUSION: Dobutamine echocardiography predicts spontaneous functional recovery after acute myocardial infarction. However, sestamibi imaging is useful to identify patients with dysfunctional myocardium without contractile reserve who may benefit from coronary revascularization.

Incremental prognostic value of thallium reinjection after stress-redistribution imaging in patients with previous myocardial infarction and left ventricular dysfunction.

UNLABELLED: This study evaluated the incremental prognostic value of 201TI reinjection imaging over clinical, exercise and thallium stress-redistribution data in patients with previous myocardial infarction and left ventricular dysfunction. METHODS: Thallium-201 reinjection after stress-redistribution SPECT was performed in 104 consecutive patients with a first Q-wave myocardial infarction (> 8 wk) and left ventricular ejection fraction < or = 40%. Follow-up data (mean 22 mo) were available for 98 patients; 16 patients underwent early revascularization procedures within 3 mo after exercise testing and were not considered for the analysis. RESULTS: During follow-up there were 13 hard events (cardiac death and myocardial infarction) and 11 soft events (coronary revascularization procedures > 3 mo after thallium imaging). With multivariate Cox regression analysis, the sum of defects at stress-redistribution imaging that were reversible or moderate irreversible after reinjection was a powerful predictor of subsequent events. The addition of thallium reinjection imaging data significantly improved the prognostic power of clinical, exercise and stress-redistribution data for the occurrence of hard events (p < 0.01). CONCLUSION: In patients with previous myocardial infarction and left ventricular dysfunction, thallium reinjection imaging provides incremental prognostic information over those obtained from conventional stress-redistribution imaging.

Comparison of verapamil versus felodipine on heart rate variability after acute myocardial infarction.

A depressed heart rate variability (HRV) is a powerful predictor of poor outcome in myocardial infarction patients. The beneficial effect of specific interventions on its recovery has been reported, but data concerning calcium antagonists are scarce. We evaluated the effect of a phenylalkylamine derivative, verapamil, and a dihydropyridine derivative, felodipine, on time- and frequency-domain measurements of HRV by 24-hour Holter monitoring in 60 patients with acute myocardial infarction (AMI). After a first Holter recording (65 +/- 8 hours from the onset of symptoms), patients were randomly assigned to continue standard treatment or to also receive verapamil retard (120 mg 3 times daily) or felodipine extended-release (10 mg/day). Holter recording was repeated after 7 days. After verapamil, mean RR interval increased from 823 +/- 92 to 907 +/- 95 ms and the SD of all normal RR (NN) intervals (SDNN) from 99 +/- 24 to 120 +/- 30 ms (p < 0.01); the root mean square successive difference (r-MSSD) and the percent of differences between adjacent NN intervals > 50 ms (pNN50) also increased (p < 0.01). After felodipine, only SDNN increased (p < 0.01). Regarding frequency-domain measurements, after receiving verapamil, very low frequency, low- and high-frequency powers increased (p < 0.01), whereas the low- to high-frequency ratio decreased (p < 0.01). After receiving felodipine, very low-frequency power increased (p < 0.01), whereas low- and high-frequency powers and the low- to high-frequency ratio remained unchanged. This study demonstrates that verapamil, but not felodipine, improves HRV in the early phase after AMI.

Usefulness of late coronary thrombolysis (recombinant tissue-type plasminogen activator) in preserving left ventricular function in acute myocardial infarction.

This study assesses whether administration of recombinant tissue-type plasminogen activator (rt-PA) up to 8 hours after onset of symptoms of acute myocardial infarction (AMI) may result in a significant improvement in left ventricular function. Sixty patients were classified into 3 groups: group A (n = 21) received rt-PA within 4 hours from symptom onset; the remaining 39 patients, admitted between 4 and 8 hours, were randomized into 2 groups--group B (n = 19) received rt-PA, and group C (n = 21) was treated with conventional therapy. Coronary and left ventricular angiograms were recorded 8 to 10 days after rt-PA administration. The patency rate of the infarct-related artery was 76% in group A, and 63 and 35% in group B and C, respectively. The Thrombolysis in Myocardial Infarction trial perfusion grade was higher in group A and B than in group C (A vs C: p less than 0.005; B vs C: p less than 0.01). Left ventricular ejection fraction was significantly higher in group A (60.2 +/- 10%) and B (54.7 +/- 12%) compared with group C (44.2 +/- 12%) (A vs C: p less than 0.01; B vs C: p less than 0.05). Regional wall motion of the entire ischemic zone was better in group A and B than in group C (A vs C: p less than 0.001; B vs C: p less than 0.01). In contrast, the kinesis of the central ischemic zone was significantly better in group A than in both group B and C (A vs B: p less than 0.05; A vs C: p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization and prognostic significance of silent myocardial ischemia on predischarge electrocardiographic monitoring in unselected patients with myocardial infarction.

Characteristics and prognostic significance of ischemic ST changes at predischarge Holter monitoring were evaluated in 270 consecutive postinfarction patients. The 64 patients with ST changes had a greater incidence of non-Q-wave myocardial infarction (p less than 0.01) and ventricular premature contractions (p less than 0.01); they were more frequently in Moss class greater than 2 (p less than 0.01) and they had a lower wall motion score (p less than 0.05). At 2-year follow-up, patients with ST changes had a higher incidence of cardiac death and reinfarction. At multivariate analysis, Killip class (p less than 0.01) and ST changes (p less than 0.05) were the most predictive variables; when multivariate analysis was repeated including an additional variable--the inability to perform a stress test--Killip class was the most significant variable (p less than 0.01), and the presence of ST changes showed only borderline statistical significance (p less than 0.1). In the subset of patients who did not perform the stress test, ST change was the most important variable (p less than 0.01), followed by Killip class (p less than 0.05). Thus, after myocardial infarction, ST changes during Holter monitoring are associated with a poor prognosis and appear useful for stratifying patients who do not perform exercise stress tests.

Continuous electrocardiographic monitoring for more than one hour does not improve the prognostic value of ventricular arrhythmias in survivors of first acute myocardial infarction.

This study was designed to compare the prognostic value of predischarge ambulatory electrocardiographic monitoring for 1, 6 and 24 hours in 188 patients surviving a first acute myocardial infarction. Ventricular premature complexes (VPCs) were considered as a mean hourly rate or classified using Lown and Moss grading systems. During the 1-year follow-up 20 cardiac deaths occurred. For all 3 monitoring times, a higher number of VPCs/hour and a higher Moss grade were associated with mortality, whereas a Lown grading system gave prognostic information only for the first hour of recording. Monitoring time did not influence specificity or sensitivity in predicting mortality; > or = 3 VPCs/hour showed a higher sensitivity than > or = 10 VPCs/hour (p < 0.05) with a comparable specificity. After 1-hour data entered the model, neither the 6- or the 24-hour data entry improved the overall likelihood ratio statistic, regardless of what VPC grading system was used. These results demonstrate that continuous electrocardiographic recordings of > 1 hour are unnecessary when they are to be used for detecting ventricular arrhythmia as a predictor of mortality in patients surviving a first acute myocardial infarction.

Cardiovascular haemodynamics and cardiac autonomic control in patients with subclinical and overt hyperthyroidism.

OBJECTIVE: To characterize cardiac structure and function and cardiac autonomic control in patients with subclinical and overt hyperthyroidism. DESIGN: Thirty patients with subclinical hyperthyroidism and 30 with overt disease were selected from patients never previously treated for endocrinological disease in the outpatient clinic of our institution. Twenty normal individuals were studied as control group. METHODS: Left ventricular structure and function and cardiac autonomic control were evaluated, respectively, by two-dimensional Doppler echocardiography and by 24-h Holter recording with heart rate variability analysis. RESULTS: Patients with overt hyperthyroidism showed greater values of left ventricular end-diastolic volume (P<0.05) and left ventricular mass (P<0.05) than patients with subclinical disease. In addition, the mean velocity of left ventricular fibre shortening (P<0.05) and left ventricular ejection fraction (P<0.05) were greater in patients with overt hyperthyroidism than in patients with subclinical disease. No difference in any of these parameters was detectable between normal subjects and patients with subclinical disease. The isovolumic relaxation period was shorter in patients with subclinical hyperthyroidism than in control individuals (P<0.05) and in patients with overt hyperthyroidism (P<0.05). As regards cardiac autonomic control, all time and frequency domain measures decreased progressively from control individuals to patients with subclinical hyperthyroidism and those with overt disease (P<0.001). CONCLUSIONS: Thyrotoxic patients show changes in left ventricular structure and increased echocardiographic indexes of myocardial contractility, whereas the only echocardiographic feature detectable in patients with subclinical hyperthyroidism is an increased velocity of left ventricular relaxation. Cardiac parasympathetic withdrawal is evident in patients with overt hyperthyroidism and in patients with subclinical disease.

Power spectral analysis of heart period variability in hypertensive patients with left ventricular hypertrophy.

This study aimed to characterize sympathovagal balance by heart period power spectrum analysis in hypertensive patients with echocardiographic evidence of left ventricular hypertrophy. Twenty ambulatory patients (11 men and 9 women), aged 50 +/- 10 years, with established essential hypertension and echocardiographic left ventricular hypertrophy, performed 24-h blood pressure monitoring and electrocardiogram Holter recording on 2 consecutive days. Twenty age- and sex-matched normal subjects comprised the control group. Power spectrum analysis, performed using the fast Fourier transform algorithm, demonstrated lower values of low and high frequency power in hypertensives than in controls, while ultralow and very low frequency power were similar in the two groups. Very low frequency, low frequency, and high frequency power increased during the night in both groups, showing a similar circadian pattern. We found a direct correlation between daytime systolic (r = 0.51; P < .05) and diastolic (r = 0.52; P < .05) blood pressure and left ventricular mass index. Moreover, negative correlations were found between left ventricular mass index and low frequency (r = -0.47; P < .05) and high frequency power (r = -0.47; P < .05). There was a direct correlation between nighttime decrease in systolic blood pressure and nighttime increase in high frequency power (r = 0.45; P < .05). As 24-h low frequency and high frequency power, obtained using the Fourier transform algorithm, both reflect the parasympathetic modulation of heart rate, our results demonstrate that hypertensive patients with left ventricular hypertrophy are characterized by a sympathovagal imbalance with a reduction of vagal tone that is more evident with increasing severity of hypertension.