Feasibility of combined percutaneous transluminal angioplasty and minimally invasive direct coronary artery bypass in patients with multivessel coronary artery disease.

BACKGROUND: Angioplasty has become an accepted treatment of patients with coronary artery disease and is now commonly used to treat patients with multivessel disease. The major disadvantage of angioplasty has been restenosis requiring repeat interventions with resultant loss of initial cost savings. Compared with the right and the circumflex coronary arteries, the left anterior descending artery (LAD) has been more adversely affected by restenosis. Recently, minimally invasive direct coronary artery bypass (MIDCAB) to the LAD through a small left anterior thoracotomy using the left internal mammary artery has been performed in some centers with excellent early results and with reduced costs compared with standard bypass surgery. METHODS AND RESULTS: We retrospectively reviewed the first 31 consecutive patients treated in our institution with integrated coronary revascularization (ICR): MIDCAB to the LAD combined with PTCA of the other diseased vessels in patients with multivessel disease. Postoperative angiography in 84% of patients revealed a patent anastomosis and normal flow in the graft and bypassed vessel. Thirty-eight (97%) of 39 vessels were successfully treated percutaneously. At a mean follow-up of 7 months, all patients are currently asymptomatic. There have been 2 adverse clinical events, both related to angioplasty and not to MIDCAB. The average length of stay at the hospital after MIDCAB was 2.79+/-1.05 days. CONCLUSIONS: These preliminary results with ICR are encouraging and suggest that a randomized, prospective clinical trial comparing ICR with standard coronary artery bypass surgery for the revascularization of symptomatic patients with multivessel disease involving the LAD is warranted.

Conjugated estrogens acutely abolish abnormal cold-induced coronary vasoconstriction in male cardiac allografts.

BACKGROUND: Transplant-associated coronary arteriopathy is manifested in its early stages by paradoxical coronary artery constriction in response to endothelium-dependent vasodilator stimuli such as the cold pressor test (CPT) and is a major cause of death or retransplantation. Estrogen has vasoactive properties that abolish coronary artery endothelial dysfunction in native hearts. We hypothesized that estrogen attenuates inappropriate coronary artery constriction in cardiac allografts. METHODS AND RESULTS: Coronary artery diameter and systemic hemodynamic responses to a 90-second CPT were measured before and 15 minutes after double-blind, randomized administration of intravenous conjugated estrogens (1.25 mg) or placebo in men with male cardiac allografts. Before estrogen, 9 men exhibited an abnormal 15.1 +/- 3.0% CPT-induced decrease in coronary artery diameter. However, repeat CPT did not induce significant coronary artery constriction when performed 15 minutes after estrogen. CPT responses before and after estrogen were significantly different (P=.02). Placebo did not influence coronary artery responses to CPT in 6 men. Systemic hemodynamic responses to CPT were not influenced by estrogen or placebo. Estrogen was the only significant determinant of changes in coronary artery responses to CPT. CONCLUSIONS: Conjugated estrogens acutely abolish abnormal CPT-induced coronary artery constriction in male cardiac allografts. This favorable vasomotor effect suggests that estrogen may prevent inappropriate coronary artery constriction in men with cardiac transplants.

Right ventricular performance and contractile reserve in patients with severe heart failure. Assessment by pressure-area relations and association with outcome.

BACKGROUND: Right ventricular (RV) performance appears to be important in patients with severe heart failure. Although clinical assessments of RV function previously have been limited to load-dependent ejection phase indices, a new method has been developed using the relatively load-insensitive concepts of pressure-volume relations with automated echocardiographic measures of RV cross-sectional area as a surrogate for volume. METHODS AND RESULTS: Sixteen patients with New York Heart Association functional class IV heart failure and group mean left ventricular ejection fraction of 20 +/- 5% were studied. RV pressure-area loops were recorded on-line from echocardiographic measures of RV area and high-fidelity pressure during transient inferior, vena caval balloon occlusions. RV contractile reserve was assessed as its functional response to an increase in dobutamine from 5.7 +/- 4.1 to 13.1 +/- 4.7 micrograms/kg per minute. Complete data sets were available in 13 patients. Group mean RV end-systolic elastance (E'es) and maximal elastance (E'max) increased with augmented dobutamine infusion (2.9 +/- 1.5 to 5.5 +/- 3.3 mm Hg/cm2 and 3.3 +/- 1.6 to 6.4 +/- 3.9 mm Hg/cm2, respectively; P < .01 versus baseline), although individual responses were variable. During a 30-day follow-up, 9 patients remained unstable, requiring continuous intravenous inotropic therapy; 6 of these had profound deterioration requiring mechanical circulatory support. The remaining 4 patients had a comparatively good short-term outcome with clinical stability. A 100% increase in RV E'es or E'max was associated with a good short-term outcome (P < .05). CONCLUSIONS: RV performance can be assessed by pressure-area relations in patients with heart failure. RV contractile reserve in response to increases in dobutamine was associated with a good short-term outcome and may be of prognostic value in patients with severe heart failure.

Predisposing risk factors and natural history of acute neurologic complications of left-sided cardiac catheterization.

The reported incidence of acute neurologic complications of left heart catheterization varies from 0.03% to 0.3%. The predisposing risk factors, clinical features, and natural history have not been well characterized. We retrospectively reviewed all cases of acute neurologic complications developing during or within 36 hours of diagnostic catheterization or angioplasty to determine the incidence, clinical features, and natural history, and (using a case-control methodology) the clinical variables associated with their development. During the 37-month study, 6,465 patients underwent diagnostic left-sided cardiac catheterization and balloon angioplasty or valvuloplasty, and 27 patients developed an acute neurologic complication (0.4%). The most common symptoms were visual disturbances (26%), hemiparesis (26%), and facial droop (26%). Deficits were localizable to the anterior or posterior circulation in 22 patients: posterior in 8 (36%), and anterior in 14 (64%). Long-term follow-up was available in all patients, with 17 of 27 (63%) having complete resolution with no residuum. With use of a case-control methodology and multiple logistic regression analysis, female gender, the presence of left ventricular hypertrophy, depressed ejection fraction, and the presence of > or = 2 coronary arteries with > 50% narrowing were independent predictors of a neurologic event.

Angioscopic evaluation of incompletely obstructing coronary intraluminal filling defects: comparison to angiography.

At 66 sites in 40 patients, we evaluated the sensitivity and specificity of coronary angiography in detecting intraluminal filling defects of varying sizes and in characterizing the contents (thrombus, intimal flap, both) of such defects using coronary angioscopy as "the gold standard." Overall angiographic sensitivity for thrombus was 37% and for intimal flap 45%. Specificity for thrombus was 100% and intimal flaps 96%. Angioscopically small flaps were less frequently seen angiographically (28%) than larger sizes (65%, p = 0.03). Angioscopically small thrombi were seen less often angiographically (30%) than larger ones (75%, p = 0.13). Filling defects (intimal flaps, thrombus, both) were characterized correctly in only 37% of sites. Angiography is relatively insensitivity in detecting intraluminal filling defects. Angioscopy may be preferred to or adjunctive with angiography in detecting these lesions.

Assessment of heart rate variability in hypertrophic cardiomyopathy. Association with clinical and prognostic features.

BACKGROUND: Altered vascular responses during exercise and disturbed responses to autonomic function testing have been documented in hypertrophic cardiomyopathy (HCM) and are associated with markers of an adverse prognosis. Reduced heart rate variability (HRV) and baroreflex sensitivity are predictors of increased risk of sudden death after myocardial infarction, but the value of these parameters in HCM is unknown. METHODS AND RESULTS: To determine the clinical significance of HRV and its relation to markers of electrical and hemodynamic instability in HCM, the 24-hour Holter recordings of 104 patients in sinus rhythm and off medication were analyzed. Five nonspectral measures of HRV were computed. The frequency components of HRV were calculated by fast Fourier transformation of the RR time intervals; the areas under the low (0.04 to 0.15 Hz) and high (0.15 to 0.4 Hz) frequency portions of the spectrum were measured as indices of autonomic and specific vagal influences on HRV, respectively. Spectral and nonspectral measures were compared with clinical, echo/Doppler, and Holter variables. ANCOVA was performed to allow for the effect of age on differences between variables. Spectral and nonspectral measures of HRV were correlated (r > .65; P < or = .001), indicating that the different time-domain and frequency parameters reflected similar measures of HRV. Global measures of HRV including the standard deviation of the mean of RR intervals (SDRR) and the standard deviation of 5-minute mean RR intervals (SDANN) were increased in patients with an adverse family history of HCM (173 +/- 67 vs 131 +/- 38 milliseconds, P = .001, and 158 +/- 66 vs 116 +/- 36 milliseconds, P = .004, respectively). In patients with exertional chest pain, global nonspectral measures were reduced compared with asymptomatic patients (118 +/- 31 vs 152 +/- 53 milliseconds, P = .006, and 105 +/- 30 vs 136 +/- 52 milliseconds, P = .014, respectively). Specific vagal influences on HRV including the proportion of RR intervals more than 50 milliseconds different (PNN50) and the high frequency peak on spectral analysis were less in patients with supraventricular arrhythmias on Holter monitoring (7.2 +/- 8 vs 16 +/- 13%, P = .012, and 21 +/- 10 vs 28 +/- 13 milliseconds, P = .048, respectively). Similarly, both global and specific vagal measures of HRV were less in the 27 patients with nonsustained ventricular tachycardia on Holter (PNN50, 7.7 +/- 9 vs 15 +/- 13 milliseconds, P = .048, and high frequency component, 19 +/- 9 vs 28 +/- 13 milliseconds, P = .05. During follow-up, 10 patients, 9 of whom were aged less than 33 years, experienced catastrophic events; 6 were resuscitated from ventricular fibrillation and 4 died suddenly. Indices of HRV were similar in these 10 patients to indices in the 94 survivors. CONCLUSIONS: Time-domain and spectral measures of HRV yield similar information about the specific autonomic influences on the heart. Global and specific vagal influences on HRV were reduced in patients with symptoms and arrhythmias and global HRV is increased in patients with an adverse family history of HCM, but these indices do not add to the predictive accuracy of established risk factors.

Increased renal and forearm vasoconstriction in response to exercise after heart transplantation.

OBJECTIVE: To test the hypothesis that the loss of the inhibitory effect of the cardiac ventricular afferent fibres on the vasomotor centre would result in increased vasoconstrictor drive to the forearm and renal vascular beds during supine exercise in heart transplant recipients. DESIGN: Comparison of regional haemodynamic response to exercise in heart transplant recipients and two age matched control groups. SETTING: Regional heart transplant unit. PATIENTS AND METHODS: Orthotopic heart transplant recipients (n = 10), patients with NYHA class II heart failure (n = 10), and normal controls (n = 10) underwent short duration maximal supine bicycle exercise. MAIN OUTCOME MEASURES: Simultaneous measurements were made of heart rate, systemic blood pressure, oxygen consumption (VO2), forearm blood flow, and renal blood flow. Forearm blood flow was measured by forearm plethysmography and renal blood flow by continuous renal vein thermodilution. RESULTS: The peak forearm vascular resistance was significantly greater in the transplant group than in the controls (mean (SEM) 75 (18) v 40 (7) resistance units, p < 0.05). The percentage fall in renal blood flow at peak exercise was significantly greater in heart transplant recipients than in the controls (44% (4%) v 32% (4%), p < 0.05) as was the percentage increase in renal vascular resistance (transplants: 116% (19%) v controls: 78% (17%), p < 0.05). Regional haemodynamics during exercise in the heart failure group were not significantly different from those in the controls. CONCLUSIONS: These findings suggest that surgical division of the cardiac ventricular afferent fibres results in increased vasoconstrictor drive to the kidneys and non-exercising muscle during exercise. This mechanism may contribute to persistent exercise limitation and renal impairment after heart transplantation.

The value of time and frequency domain, and spectral temporal mapping analysis of the signal-averaged electrocardiogram in identification of patients with hypertrophic cardiomyopathy at increased risk of sudden death.

Late potentials detected by the signal-averaged ECG (SAECG) identify post-infarction patients at risk from sustained ventricular tachycardia (VT) and sudden death. Hypertrophic cardiomyopathy (HCM) is also associated with increased risk of sudden death. In adults, episodes of non-sustained VT on ambulatory ECG monitoring are a marker of high risk patients. In children and adolescents, however, there is no reliable ECG marker, and clinical features have low predictive accuracy. The prognostic value of the SAECG in HCM has not been systematically evaluated. We examined the relation of detailed time domain, frequency domain, and spectral temporal mapping analysis of the SAECG and clinical and echocardiographic features, and the results of 48 h ambulatory ECG monitoring in 121 consecutive patients with HCM. Non-sustained VT on Holter monitoring was recorded in 27 (23%) patients. An abnormal time domain SAECG was present in three (11%) patients with VT vs three (3%) without VT (ns). Of the SAECG variables, reduced (below 150 microV) voltage of the initial 40 ms of the signal-averaged QRS complex was the best predictor for non-sustained VT (sensitivity: 95%; specificity: 74%: positive predictive accuracy: 64%; negative predictive accuracy: 97%). Nine patients (of whom eight were < or = 30 years of age) experienced catastrophic events: three died suddenly and six had been resuscitated from out-of-hospital ventricular fibrillation. None of them had an abnormal time domain SAECG. The frequency domain analysis and spectral temporal mapping of the SAECG did not improve the identification of patients with VT or patients with catastrophic events. In conclusion, alterations of the initial portion of the signal-averaged QRS complex identified patients with HCM and non-sustained VT, but the SAECG was not useful in identifying young patients who suffered cardiac arrest.

Regional thallium-201 washout and myocardial hypertrophy in hypertrophic cardiomyopathy and its relation to exertional chest pain.

The mechanism of exertional chest pain in hypertrophic cardiomyopathy is uncertain, but may relate to myocardial ischemia. To study the mechanism of exertional chest pain in hypertrophic cardiomyopathy, dipyridamole-stress thallium-201 single-photon emission computed tomography was performed in 82 consecutive patients, and the 3-hour washout of thallium in relation to the tomographic image, regional wall thickness on echocardiography, and other clinical findings was analyzed. There was a weak inverse correlation of regional washout and wall thickness in 298 analyzed quadrant areas (r = -0.29; p = 0.0001). Twenty-five patients (31%) had history of exertional chest pain, and showed a significantly lower total washout and greater maximal left ventricular wall thickness than did those without chest pain (32 +/- 10% vs 37 +/- 9% [p = 0.03], and 27 +/- 7 vs 23 +/- 7 mm [p = 0.03], respectively). Even in mildly and nonhypertrophied areas, patients with chest pain had a significantly lower regional washout than did those without pain (33 +/- 10% vs 38 +/- 9%; p = 0.02), despite similar left ventricular wall thickness (12 +/- 2 vs 11 +/- 3 mm; p = NS). Reduced washout was strongly associated with exertional chest pain and was observed in myocardial regions that had normal as well as increased thickness, which indicates that this abnormality of thallium kinetics is a function of the disease process and not the magnitude of left ventricular hypertrophy.

Assessment of autonomic function in patients with neurally mediated syncope: augmented cardiopulmonary baroreceptor responses to graded orthostatic stress.

OBJECTIVES: The purpose of this study was to assess vagal tone and cardiopulmonary baroreceptor activity in patients with tilt-induced neurally mediated syncope. BACKGROUND: The causes of individual susceptibility to orthostatic stress leading to recurrent neurally mediated syncope remain obscure. The trigger for sympathetic withdrawal and increased vagal activity is believed to be stimulation of ventricular mechanoreceptors. METHODS: Seventeen patients (mean age 50.6 years) with recurrent syncope and a positive response on a 45-min 60 degrees head-up tilt test were compared with a control group of 17 patients (mean age 47.5 years) with unexplained syncope and negative tilt test findings. Vagal activity was assessed by high pressure baroreceptor testing and by temporal and spectral analysis of heart rate variability during Holter ambulatory electrocardiographic monitoring. Cardiopulmonary baroreceptor sensitivity was assessed by measurement of forearm vascular responses to lower body negative pressure. RESULTS: Mean high pressure baroreceptor sensitivity was 16.4 +/- 12.2 ms/mm Hg in the group with a positive tilt test response compared with 15.1 +/- 13.0 ms/mm Hg in the control group (p = NS). There were no significant differences between the groups in any of the temporal or spectral measures of heart rate variability. The increase in forearm vascular resistance in response to lower body negative pressure was 11.5 +/- 14.2 U in patients with tilt-induced syncope and 3.5 +/- 3.2 U in the control group at -5 mm Hg, 16.8 +/- 18.6 U and 4.8 +/- 5.3 U, respectively, at -10 mm Hg and 26.4 +/- 24.3 U and 10.2 +/- 7.8 U, respectively, at -20 mm Hg (p < 0.001). CONCLUSIONS: Patients with tilt-induced neurally mediated syncope have augmented cardiopulmonary baroreceptor responses to orthostatic stress. This finding sheds new light on the etiology of neurally mediated syncope.

Impaired immediate vasoconstrictor responses in patients with recurrent neurally mediated syncope.

Immediate responses to head-up tilt were determined in 78 consecutive patients with unexplained syncope undergoing 45-minute tilt tests at 60 degrees. Thirty-four patients developed neurally mediated syncope (mean time to syncope 18 minutes), 40 tolerated the full duration of tilt, and 4 were unable to complete the study but did not develop syncope. Blood pressure, heart rate, forearm blood flow and forearm vascular resistance were measured at baseline and after 2 and 5 minutes of tilt. Syncopal and nonsyncopal patients were well-matched for age and baseline hemodynamic parameters. There was no difference between the groups in heart rate or blood pressure at 2 minutes, but there was a small but significant difference in percent reduction in mean arterial pressure at 5 minutes. After 2 and 5 minutes of tilt, mean forearm blood flow was 2.4 and 2.6 ml/min/100 ml, respectively, in syncopal patients compared with 1.6 (p < 0.05) and 1.7 ml/min/100 ml (p < 0.01), respectively, in patients who tolerated 45 minutes of tilt. In syncopal patients, forearm vascular resistance was 51.0 and 44.0 at 2 and 5 minutes, respectively, whereas in nonsyncopal patients, it was 82.4 (p < 0.02) and 73.1 (p < 0.001), respectively. These differences remained consistent when only data for patients developing syncope after > 15 minutes were included in the analysis. Patients with neurally mediated syncope have clearly demonstrable abnormalities in vascular control immediately after assumption of the upright posture. The results shed new light on the pathophysiology of neurally mediated syncope.

Validation of bedside measurements of absolute human renal blood flow by a continuous thermodilution technique.

BACKGROUND AND METHODS: There is a clinical need for a system that would allow rapid assessment of renal blood flow in patients with oliguric circulatory shock. A local, continuous thermodilution technique for the measurement of renal venous blood flow, using readily available equipment, was developed. To test the hypothesis that this system would allow measurement of renal blood flow in clinical situations, we compared simultaneous measurements made by the continuous thermodilution technique with measurements of: a) absolute flow measured by volumetric collection in an in vitro flow model; b) renal arterial blood flow measured by electromagnetic flow probe under changing hemodynamic conditions in nine pigs; and c) calculated renal blood flow derived from a clearance technique in 16 patients after cardiac catheterization. The technique utilizes a short-duration, constant infusion of room temperature normal saline into the renal vein via a retrograde thermodilution catheter, with measurement of flow at a thermistor 1 cm back from the tip of the catheter. RESULTS: The method measured absolute blood flow in an in vitro model, with a correlation coefficient of .99 over blood flows ranging from 55 to 885 mL/min (r2 = .98). There was a .92 correlation coefficient with renal arterial blood flow measured by electromagnetic flow probe in a pig model (r2 = .85), and a .8 correlation with simultaneous measurement of renal blood flow by corrected iodohippurate clearance in humans (r2 = .64). Compared with electromagnetic flow probe measurements, a single measurement by the thermodilution technique would be accurate to within 80 mL/min in 95% of cases. Variability between individual measurements, expressed as the mean of the coefficient of variance for each patient, was 5.5 +/- 3.7%. CONCLUSIONS: This technique is simple to use, requires only venous cannulation and injection of normal saline, and allows rapidly repeatable, immediately available measurements of renal blood flow in a wide range of clinical circumstances, including severe renal impairment or anuria.

Effects of amiodarone on erect and supine exercise haemodynamics and exercise capacity in patients with hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a primary heart muscle disease associated with a high incidence of sudden death. Amiodarone is of benefit in those patients with a high risk profile for sudden death. Amiodarone has also been reported to improve symptoms dramatically in some patients with HCM but to cause functional deterioration in others. In the acute phase of oral amiodarone therapy there are few discernable changes in cardiovascular haemodynamics and the mechanisms of any beneficial effects on symptoms remain unclear. To determine the effect of amiodarone on exercise responses we measured haemodynamic indices in 10 patients during maximal supine- and symptom-limited erect treadmill exercise before and 6 weeks after amiodarone therapy. Following amiodarone therapy there was a significant reduction in resting and peak heart rate during erect exercise (76 +/- 13 vs 97 +/- 19 b.min-1; P = 0.001 and 114 +/- 26 vs 146 +/- 21 b.min-1; P = 0.001 respectively). Despite increases in peak pulmonary and systemic artery pressures with amiodarone therapy there was no difference in the peak left ventricular filling pressure or maximum cardiac output achieved. Similarly, during supine exercise the resting and peak heart rates were less following the 6 weeks amiodarone therapy. Comparison of supine and erect exercise haemodynamic indices demonstrated higher peak LV filling and higher peak systolic and pulmonary artery pressures during supine than during erect exercise (29 +/- 10 vs 25 +/- 12; P less than 0.04; 151 +/- 42 vs 126 +/- 48; P = 0.01 and 66 +/- 27 vs 62 +/- 21; P = 0.08 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of exercise limitation in hypertrophic cardiomyopathy.

To assess the relation of exercise capacity to indexes of systolic and diastolic function in hypertrophic cardiomyopathy, 81 patients underwent two-dimensional echocardiography, technetium-99m equilibrium radionuclide angiography acquired in list mode and maximal, symptom-limited, treadmill exercise testing with measurement of maximal oxygen consumption (VO2 max). VO2 max for the group was 13.9 to 49.3 (mean 25.4) ml/min per kg. Thirty-six patients (44%) achieved less than or equal to 70% of age-predicted VO2 max. Patients with such a degree of limitation were more likely to be in New York Heart Association functional class II or III (23 of 36 vs. 14 of 45; p = 0.005); there was no such relation between VO2 and the incidence and magnitude of rest left ventricular outflow tract pressure gradient greater than 30 mm Hg (11 of 36 vs. 11 of 45; p = NS and 58 +/- 24 vs. 65 +/- 19 mm Hg; p = NS). In the 22 patients with a left ventricular outflow tract gradient, the ratios of peak ejection to peak filling rate and of atrial contribution to left atrial dimension were related to percent of the age-predicted VO2 max (r = 0.49, p = 0.02 and r = 0.54, p less than 0.02). These ratios reflect impaired left ventricular systolic performance and atrial systolic failure, respectively. Stepwise discriminant analysis revealed these two ratios to be the two strongest predictors (p = 0.0001) of patients with a left ventricular outflow tract gradient whose VO2 max was less than or equal to 70% of the age-predicted value (sensitivity 90%, specificity 100%).(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormal vascular responses to supine exercise in hypertrophic cardiomyopathy.

BACKGROUND: Exercise hypotension has been documented in hypertrophic cardiomyopathy. It is not the result of an inability to augment cardiac output but instead relates to an inappropriate and exaggerated decrease in systemic vascular resistance at high work loads. METHODS AND RESULTS: To enable us to examine the behavior of the peripheral vasculature during exercise, 103 consecutive patients underwent maximal symptom-limited supine bicycle exercise with measurement of forearm blood flow. A minimum reduction of 12% from the basal value was defined as a normal response based on the study of 25 normal controls. In the patients, two patterns of forearm blood flow were observed. Sixty-four patients had an appropriate reduction in forearm blood flow of 40 +/- 16% from resting flow. In 39 patients, the forearm blood flow either failed to decrease or increased with exercise by 45 +/- 105% of the resting value. Patients with an abnormal forearm vasodilator response were younger (31 +/- 13 versus 46 +/- 14 years), and more of them had a family history of hypertrophic cardiomyopathy and sudden death than did those with a normal vasoconstrictor response (16 of 39 versus eight of 64). Left ventricular end-diastolic cavity dimensions were smaller in those with an abnormal forearm blood flow response, but other clinical, echocardiographic, and arrhythmic variables were similar. To assess the relation of abnormal peripheral vascular responses to erect exercise blood pressure response, patients underwent treadmill exercise testing with careful monitoring of systolic blood pressure response. Thirty-eight patients had significant exercise hypotension with failure of the systolic blood pressure to increase during progressive exercise (n = 6) or an abrupt decrease in systolic blood pressure (20-60 mm Hg) from the peak value (n = 32); 65 patients had a normal exercise blood pressure response, but 18 of these patients had an oscillation in systolic blood pressure of 10 mm Hg or more early in the recovery phase. Thirty-one of 39 patients with an abnormal forearm blood flow response demonstrated exercise hypotension during the erect exercise testing, and the remaining eight patients had a normal exercise blood pressure response; however, five of these eight had abnormal oscillations in blood pressure during recovery (r = 0.61, p less than 0.001). CONCLUSIONS: The relation of abnormal peripheral vascular responses to exercise hypotension confirms the observation of hemodynamic instability in patients with hypertrophic cardiomyopathy. The finding of abnormal vascular responses in patients known to be at increased risk (young age and a family history of hypertrophic cardiomyopathy and sudden death) suggests that hemodynamic mechanisms may be important in the occurrence of sudden death in hypertrophic cardiomyopathy.

Infective endocarditis in a heart transplant recipient.

A 38-year-old man underwent orthotopic heart transplantation because of heart failure caused by ischemic heart disease. Three months after the operation cholestatic jaundice related to azathioprine hepatotoxicity developed, necessitating supplementation of cyclosporine immunosuppression with prednisolone. Seven months after heart transplantation he had a septic right femoral embolus and, by transesophageal echocardiography, was found to have a vegetation on the anterior leaflet of the mitral valve. Treatment with appropriate antibiotics resulted in complete resolution of symptoms and healing of the vegetation. Six months after the episode he remains free of symptoms and has normal heart function.

Abnormal blood pressure response during exercise in hypertrophic cardiomyopathy.

To investigate the incidence of abnormal exercise blood pressure responses in hypertrophic cardiomyopathy (HCM) and the potential role of hemodynamic instability as a mechanism of sudden death, 129 consecutive patients with HCM underwent maximal symptom-limited treadmill exercise testing with blood pressure recording. Four patterns of blood pressure response were observed. Forty-three patients had significant exercise hypotension, with either a continuous fall in systolic blood pressure (n = 5) from the start of exercise or a sudden fall in systolic blood pressure (20-100 mm Hg; mean, 40 mm Hg) from the peak value (n = 38), 23 patients had a normal response during exercise but an abnormal blood pressure response in the recovery period, and the remaining 62 patients demonstrated a normal blood pressure response. Patients with exercise hypotension were younger (33 +/- 14 versus 46 +/- 14 years) and more of them had a family history of HCM and sudden death compared with those with a normal blood pressure response (15 of 43 versus 6 of 62 patients). Similarly, the 23 patients with abnormal recovery blood pressure responses were younger (43 +/- 16 versus 46 +/- 14 years) and had a higher incidence of a family history of sudden death (10 of 24 versus 6 of 62 patients). Left ventricular cavity dimensions were smaller in those with exercise hypotension, but 11 other clinical, echocardiographic, and arrhythmic variables were similar. To assess the mechanism of exercise hypotension, 14 patients who demonstrated exercise hypotension and 14 symptomatic patients with a normal exercise blood pressure response underwent invasive hemodynamic exercise testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Risk-benefit assessment of amiodarone in the treatment of cardiac arrhythmias.

Cardiac arrhythmias are a cause of significant morbidity and mortality in patients with cardiac disease, and thus represent a major management problem. The recognition that antiarrhythmic drugs have the potential to aggravate as well as to attenuate arrhythmias has prompted clinicians to reconsider treatment strategies and weight the benefits of treatment against the risks. In this context, amiodarone has emerged as an effective antiarrhythmic agent and when used at the lowest effective dose has an acceptable side effect profile. This review focuses on the current clinical usage of amiodarone in a broad variety of cardiac arrhythmias, and addresses the risk-benefits arising from its use. It further discusses the current position of amiodarone in the management of sudden cardiac death.