Abnormal Exercise Blood Pressure Research Articles

Management and outcomes of hypertrophic cardiomyopathy in young adults

Management of young adults with hypertrophic cardiomyopathy (HCM) is challenging. To evaluate the profile of young adults (16-25 years) with HCM included in the French prospective HCM registry. Patients were compared according to occurrence of major adverse cardiac events (MACE), comprising sudden cardiac death (SCD) events (implantable cardioverter defibrillator [ICD] discharge, SCD, sustained ventricular tachycardia), atrial fibrillation/embolic stroke, heart failure hospitalisation and unexplained syncope, at a mean follow-up of 4.4±2.2 years. At baseline, among 61 patients (20.5±3.0 years; 16 women, 26.2%), 13 (21.3%) had a prophylactic ICD, 24.6% a family history of SCD, 29.5% obstruction, 86.0% magnetic resonance imaging myocardial fibrosis, 11.8% abnormal exercise blood pressure and 52.8% a European Society of Cardiology (ESC) 5-year SCD score<4% (24.5%≥6%). At follow-up, 15 patients (24.6%; seven women; all with fibrosis) presented 17 MACE, comprising: SCD events (n=7, 41.2%; including three patients with an ICD, five with at least one SCD major classical risk factor and an ESC score≥5% and two with no risk factors and an ESC score<4%); atrial fibrillation/stroke (n=6, 35.3%); heart failure (n=1, 5.9%); syncope (n=3, 17.6%). An ICD was implanted in 11 patients (four for secondary prevention), but in only 61.5% of patients with a score≥6%. Only obstruction significantly increased MACE risk (odds ratio 3.96; P=0.035), with a non-significant trend towards a lower risk in men (OR 0.29; P=0.065). In young adults with HCM, MACE are common in the short term, especially in obstructive HCM and women, mostly arrhythmic in origin. Prophylactic ICD implantation is frequent and does not strictly follow the guidelines, while the use of European/USA guidelines is helpful but imperfect in identifying SCD risk.

Hypertrophic cardiomyopathy (HCM) in the young adult: Data from the REMY register of the French Society of Cardiology

Hypertrophic cardiomyopathy (HCM) is considered to be the first cause of sudden death in young subjects, including competitive athletes, often in the absence of significant symptoms. However, most of these data come from tertiary centers and the clinical profile of these patients, as well as their management in real life in France, remain poorly understood. To evaluate the management of young adults with sarcomeric HCM and the predictive factors for major cardiac event (MCE), patients < 25 years included in the national HCM register “REMY” of the French Society of Cardiology from 2006 to 2018 were identified. At inclusion was calculated the European 5-year sudden cardiac death (SCD) score and identified the presence of the 5 major classical SCD risk factors (MRF). At follow-up, MCE [SCD or implantable cardioverter defibrillator (ICD) shock, sustained ventricular tachycardia (SVT), atrial fibrillation (AF), stroke, hospitalization for heart failure (HFH) or syncope] were notified. Among 61 included patients [20.5 ± 3(16–25) years, 16(26%) women], 92% were in NHYA class I/II, 18(30%) obstructive, 37(86%) showed MRI fibrosis, 6(12%) abnormal exercise blood pressure response, 25% a family history of SCD, 13(21%) had a prophylactic ICD. The score (4.8 ± 3.2%) was < 4% in 53% and ≥ 6% in 25% of patients. After 4.4 ± 2.2years, 15(25%) patients (7 women) presented 18 MCE: 3 SCD (17%), 5 SVT (28%), 5 AF and 1 stroke (33%), 1 HFH (5%), 3 unexplained syncopal episodes (17%); 10 patients received an ICD (4 in secondary prevention). 61% patients with score> 6% had an ICD. Female sex was predictive of MCE ( P = .02), with a tendency for obstruction ( P = .09), but not late gadolinium enhancement, prophylactic ICD or MRF. Thus, in young adults with HCM, MCE are common, especially in women, more often rhythmic. Prophylactic ICD is frequent, especially if the score exceeds 6%, but MCE are difficult to predict using the current criteria.

P990Assessment of clinical risk factors for all-cause mortality among hypertrophic cardiomyopathy patients with ICDs

Abstract Introduction According to the literature, the annual mortality rate of hypertrophic cardiomyopathy (HCM) patients is estimated to 1–2%. Sudden cardiac death (SCD), heart failure and thromboembolism are the main causes of death among this population. Patients at high risk for SCD, identified using HCM risk score, are qualified for ICD implantation. Unfortunately for clinicians, there is no validated model or statistical tool for assessment of the risk of mortality within the HCM patients with ICDs. Purpose The aim of this study was to determine the main risk factors of all- cause mortality in HCM patients with ICDs. Methods The long-term follow-up of group of 104 consecutive patients with HCM, who had the ICD implanted between 1996 and 2006 in tertiary reference clinical unit was performed. Twenty patients who died during observation were the subject of the current analysis. ICD was implanted for primary (n=16) and secondary (n=4) prevention of SCD within this subpopulation. Analysis were performed for mentioned below potential risk factors: age at the time of implantation, syncopes, family history of SCD, atrial fibrillation/supraventricular tachycardia, decreased left ventricular ejection fraction (LVEF), non-sustained ventricular tachycardia (nsVT), maximum left ventricular wall thickness, abnormal exercise blood pressure response, left ventricular outflow tract obstruction. Results The average time of survival since ICD implantation was 8,5±4,6 years. Decreased LVEF (Wald chi2 4,57; p=0,033), secondary prevention (Wald chi2 8,57; p=0,003), family history of SCD (Wald chi2 4,93; p=0,026) and episodes of nsVT (Wald chi2 3,49; p=0,062) are the clinical risk factors that significantly affect the time of survival. The probability of death, expressed as Hazard Ratio, was 27-fold higher in secondary prevention group (HR=27,18), almost 10-fold higher in patients with positive family history of SCD (HR=9,74) and 3,7-fold higher when nsVT was detected. The cause of death was established in 16/20 patients. In 15 cases, these were deaths from cardiovascular causes: end-stage heart failure (8), complications of heart transplantation or circulatory support (4), SCD (1) and other cardiovascular (2). Conclusion Secondary prevention, positive family history of SCD, nsVT and decreased LVEF seem to be the most significant risk factors associated with all- cause mortality in HCM patients with ICDs. Despite the ICD implantation, subpopulation studied had poor prognosis with high incidence of progression to end-stage heart failure. Further studies to create validated model for assessment of death risk in long-term observation of patients with HCM after ICD implantation are required.

Abnormal stress echocardiography findings in cardiac amyloidosis

Background: Cardiac involvement in immunoglobulin light chain (amyloid light chain, AL) amyloidosis is characterized by myocardial interstitial deposition but can also cause obstructive deposits in the coronary microvasculature.Methods: We retrospectively identified 20 patients who underwent stress echocardiography within 1 year prior to the histologic diagnosis of AL amyloidosis. Only patients with cardiac amyloidosis and no known obstructive coronary disease were included.Results: Stress echocardiograms (13 exercise; 7 dobutamine) were performed for evaluation of dyspnea and/or chest pain. Stress-induced wall motion abnormalities (WMAs) occurred in 11 patients (55%), 4 of whom had normal left ventricular wall thickness. Coronary angiogram was performed in 9 of 11 patients and demonstrated no or mild epicardial coronary artery disease. Seven (54%) patients had an abnormal exercise blood pressure which occurred with similar likelihood between those with and without stress-induced WMAs.Conclusions: Stress-induced WMAs and abnormal exercise blood pressure may occur in patients with cardiac AL amyloidosis despite the absence of significant epicardial coronary artery disease. This finding should raise the possibility of cardiac amyloidosis even in the absence of significant myocardial thickening.

Sudden Cardiac Death in Young Adults

Sudden cardiac death is defined as death from unexpected circulatory arrest resulting from cardiac arrhythmia which occurs within one hour of the onset of symptoms. Hypertrophic cardiomyopathy (HCM) is the leading cause of sudden cardiac death in young athletes in the United States and the most common genetic cardiovascular disorder. HCM is characterized by a heavy muscular hyper contracting heart and is a diastolic disorder of heart with asymmetric hypertrophy of ventricular septum. HCM is mostly asymptomatic until sudden cardiac death occurs. Sudden death due to cardiac failure is the most common cause of death and particularly likely in young males with familial HCM or with a family history of sudden death. Major risk factors for sudden death in individuals with Hypertrophic cardiomyopathy include prior history of cardiac arrest, ventricular fibrillation, spontaneous sustained ventricular tachycardia, family history of premature sudden death, unexplained syncope, left ventricular thickness more than or equal to 30mm, abnormal exercise blood pressure and non-sustained ventricular tachycardia. We are hereby reporting few rare cases of sudden cardiac deaths, the bodies of which were brought to the mortuary of S.C.B Medical College, Cuttack for autopsy.

Circulating Matrix Metalloproteinases in Adolescents With Hypertrophic Cardiomyopathy and Ventricular Arrhythmia

Myocardial fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM) and a risk factor for ventricular arrhythmia. Fibrosis can be reflected in circulating matrix remodeling protein concentrations. We explored differences in circulating markers of extracellular matrix turnover between young HCM patients with versus without history of serious arrhythmia. Using multiplexed and single ELISA, matrix metalloproteinases (MMPs) 1, 2, 3, and 9; tissue inhibitor of metalloproteinases (TIMPs) 1, 2, and 4; and collagen I carboxyterminal peptide (CICP) were measured in plasma from 45 young HCM patients (80% male patients; median age, 17 years [interquartile range, 15-20]). Participants were grouped into serious ventricular arrhythmia history (VA) versus no ventricular arrhythmia history (NoVA). Differences in MMPs between groups were examined nonparametrically. Relationships between MMPs and ventricular arrhythmia were assessed with linear regression, adjusted for interventricular septal thickness, family history of sudden death, abnormal exercise blood pressure, and implantable cardioverter-defibrillator (ICD). In post hoc sensitivity analysis, age was substituted for ICD. The 14 VA patients were older than 31 NoVA patients (median, 19 versus 17 years; P=0.03). All 14 VA and 12 NoVA patients had an ICD. MMP3 concentration was significantly higher in the VA group (VA median, 12.9 μg/mL [interquartile range, 5.7-16.7 μg/mL] versus NoVA, 5.8 μg/mL [interquartile range, 3.7-10.0 μg/mL]; P=0.01). On multivariable analysis, VA was independently associated with increasing MMP3 (standardized β, 0.37; P=0.01). Post hoc adjustment for age attenuated this association. Circulating MMP3 may be a marker of ventricular arrhythmia in adolescent patients with HCM. Because of our role as pediatric providers, we cannot exclude age-related confounding.

Contribution of autonomic dysfunction to abnormal exercise blood pressure in type 2 diabetes mellitus

ObjectivesThe purpose of this study was to compare the presence and severity of autonomic dysfunction in type 2 diabetes mellitus patients, with and without exaggerated blood pressure responses to exercise. DesignWe performed a cross-sectional analysis of 98 patients with type 2 diabetes mellitus (aged 59±9). MethodsBoth time (standard deviation of RR intervals, root-mean-square of successive RR interval differences) and frequency (total spectral power, high frequency, low frequency, very low frequency) domains of heart rate variability were analysed in a 5min recording at rest and 20min after a maximal treadmill test. An exaggerated blood pressure response to exercise was identified by peak blood pressure ≥190/105mmHg (women) or ≥210/105mmHg (men). ResultsEach group of either exaggerated exercise blood pressure response or normal blood pressure response consisted of 49 patients. At rest there were no significant differences between groups for all time and frequency domain parameters of heart rate variability. Post-exercise, there was a significant (p<0.05) reduction in the SDNN, RMSSD and TP in the exaggerated exercise blood pressure group. Independent correlates (p<0.01) of exercise systolic blood pressure included post-exercise TP, resting systolic blood pressure, cardiac autonomic neuropathy and beta-blockers (beta=−0.28, adj. R2=0.32, p<0.001). ConclusionsReduced post-exercise heart rate variability in patients with type 2 diabetes mellitus, with an exaggerated exercise blood pressure response suggests preclinical autonomic dysfunction characterized by impaired vagal modulation.

Contribution of autonomic dysfunction to abnormal exercise blood pressure in patients with type 2 diabetes mellitus

Contribution of autonomic dysfunction to abnormal exercise blood pressure in patients with type 2 diabetes mellitus

Abnormal exercise blood pressure predicts left ventricular mass in pre-hypertensive, middle-aged men and women

An abnormal rise in systolic blood pressure (SBP) during exercise is associated with left ventricular hypertrophy (LVH). However, this association and the magnitute of change in exercise SBP is not defined in pre-hypertensives. We assessed cardiac structure (echocardiography) and exercise parameters (BP) in middle-aged pre-hypertrensive men (n=296; age=49±10) and women (n=243; age=54±10yrs) free from heart disease, to determine the association between left venricular structure and exercise BP. LVH was defined as LVM Index≥116g/m2 for men and ≥105g/m2 for women. The prevalence of LVH was 53% in pre-hypertensive women and 21% in men. Significant correlations were noted between LVMI and exercise capacity. Multiple regression analysis (stepwise) revealed that SBP at 6 min of exercise (7METs), age and exercise capacity were the strongest predictors of LVMI for pre-hypertensive men (R2=0.52) and women (R2=0.53). Cut-off analysis revealed that the 6-min SBP threshold for LVH was ≥164 mmHg for men and ≥169 mmHg for women. LVH was present in about 86% of women and 59% of men who reached their respective BP threshold. There was approximately a 6-fold increase in the likelihoood of having LVH in men and 2.9-fold increase in women for every 10 mmHg increase in SBP above these thresholds. Significantly higher LVMI values were also noted in those who met or exceeded the respective SBP threshold vs those who did not (120±23g/m2 vs 92±11g/m2 p=0.000) for men and (133±25g/m2 vs 96±15g/m2; p=0.000) for women respectively. 1) The prevalence of LVH is 2.5 times higher in pre-hypertensive women than men. 2) SBP at 6 min of exercise, predicts LVH in pre-hypertensive men and women. 3) The SBP threshold for LVH is ≥169 mmHg for women and ≥164 mmHg for men. 4) The likelihood of having LVH increases by 6-fold for every 10 mmHg increase above this threshold for men and 2.9-fold for women.

Nondippers have higher incidence of abnormal exercise blood pressure response left ventricular hypertrophy and diastolic dysfunction in pre-hypertensive and hypertensive men

Nondippers have higher incidence of abnormal exercise blood pressure response left ventricular hypertrophy and diastolic dysfunction in pre-hypertensive and hypertensive men

Approach to hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy is a genetic disease characterized by marked left ventricular (LV) hypertrophy. A dynamic LV outflow obstruction is present in approximately 20% of patients. Many affected individuals remain asymptomatic throughout life, others develop heart failure symptoms or atrial fibrillation (AF), and some die suddenly, often young and in the absence of previous symptoms. Stratification of sudden death risk is based on several markers, including a previous cardiac arrest, sustained ventricular tachycardia, family history of sudden death, extreme LV hypertrophy (>/= 30 mm), syncope, nonsustained ventricular tachycardia on Holter, and abnormal exercise blood pressure response. The implantable cardioverter-defibrillator is the most effective treatment for sudden death prevention, and should be considered in patients with either one strong or multiple risk factors. Important symptoms of heart failure develop in a minority of patients, largely as a consequence of diastolic dysfunction, and are usually treated with beta blockers, or verapamil. In patients with LV obstruction and severe symptoms unresponsive to medications, myectomy operation or alcohol septal ablation is indicated for relieving the gradient and improving quality of life. AF develops in approximately 20% of patients. Amiodarone is the most effective medication for preventing AF recurrences. In chronic AF, beta blockers or verapamil are usually effective for heart rate control. The threshold for anticoagulants is low, because even brief AF episodes have a substantial embolization risk.

Management strategies in hypertrophic cardiomyopathy: influence of age and morphology

Management in hypertrophic cardiomyopathy is aimed at improving symptoms and exercise capacity and preventing complications, particularly sudden death. The strategy for management of symptoms is to identify potentially important mechanisms at which treatment can be targeted. Assessment is feasible with non-invasive evaluation. All patients with hypertrophic cardiomyopathy should undergo risk assessment for sudden death, regardless of their symptomatic, morphological and haemodynamic status. Recent prospective studies have examined five risk markers: family history of sudden death (two or more members aged <45 years), unexplained syncope, non-sustained ventricular tachycardia on Holler monitoring, abnormal exercise blood pressure response and severe left ventricular hypertrophy (≥3 cm). The majority of patients had none of these risk factors and did not die suddenly. Annual sudden death rates were at least 2% among patients with two or more of these risk markers, which warrants consideration of prophylactic treatment (amiodarone, implantable cardioverter-defibrillator) in such patients.

Survival after cardiac arrest or sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy

OBJECTIVESThe aim of this study was to evaluate the survival of patients with hypertrophic cardiomyopathy (HCM) after resuscitated ventricular fibrillation or syncopal sustained ventricular tachycardia (VT/VF) when treated with low dose amiodarone or implantable cardioverter defibrillators (ICDs).BACKGROUNDProspective data on clinical outcome in patients with HCM who survive a cardiac arrest are limited, but studies conducted before the widespread use of amiodarone and/or ICD therapy suggest that over a third die within seven years from sudden cardiac death or progressive heart failure.METHODSSixteen HCM patients with a history of VT/VF (nine male, age at VT/VF 19 ± 8 years [range 10 to 36]) were studied. Syncopal sustained ventricular tachycardia/ventricular fibrillation occurred during or immediately after exertion in eight patients and was the initial presentation in eight. One patient had disabling neurologic deficit after VT/VF. Before VT/VF, two patients had angina, four had syncope and six had a family history of premature sudden cardiac death. After VT/VF all patients were in New York Heart Association class I or II, three had nonsustained VT during ambulatory electrocardiography and 11 had an abnormal exercise blood pressure response. After VT/VF eight patients were treated with low dose amiodarone and six received an ICD. Prophylactic therapy was declined by two patients.RESULTSMean follow-up was 6.1 ± 4.0 years (range 0.5 to 14.5). Cumulative survival (death or ICD discharge) for the entire cohort was 59% at five years (95% confidence interval: 33% to 84%). Thirteen (81%) patients were alive at last follow-up. Two patients died suddenly while taking low dose amiodarone, and one died due to neurologic complications of his initial cardiac arrest. Three patients had one or more appropriate ICD discharges during follow-up; the times to first shock after ICD implantation were 23, 197 and 1,124 days.CONCLUSIONSThis study shows that patients with HCM who survive an episode of VT/VF remain at risk for a recurrent event. Implantable cardioverter defibrillator therapy appears to offer the best potential benefit regarding outcome.

Improvement in exercise capacity and exercise blood pressure response after transcoronary alcohol ablation therapy of septal hypertrophy in hypertrophic cardiomyopathy

Transcoronary alcohol ablation (TAA) therapy of septal hypertrophy was recently proposed as a therapeutic modality for obstructive hypertrophic cardiomyopathy (HC). However, questions remain about the effect of TAA on exercise performance. We performed a time-course analysis of exercise capacity and exercise hemodynamics in 20 patients with symptomatic obstructive HC after TAA. Symptom-limited bicycle exercise testing was performed before and 3 and 12 months after TAA, and cardiac catheterization at 3-month follow-up. The pressure gradient of the left ventricular outflow tract immediately decreased from 58 ± 8 to 4 ± 1 mm Hg at rest (p <0.01) and from 143 ± 11 to 30 ± 6 mm Hg after extrasystole (p <0.01), but partially recovered at 3-month follow-up (14 ± 4 and 40 ± 9 mm Hg, respectively). Left ventricular end-diastolic pressure was not changed after TAA. Peak oxygen consumption increased from 19 ± 2 to 23 ± 1 ml/kg/min (p < 0.01) and exercise duration from 573 ± 47 to 742 ± 46 seconds (p <0.01) at 3-month follow-up, but thereafter reached a plateau. Abnormal patterns of exercise blood pressure response were shown in 9 patients but normalized after TAA. Major complications occurred in 4 patients: no reflow to the left anterior descending coronary artery in 2 patients and ventricular tachycardia requiring cardioversion in 2 patients. During the follow-up period, all patients survived with symptomatic improvement in 17 patients. Thus, TAA is a promising therapeutic modality with improvement in exercise capacity and abnormal exercise blood pressure response in obstructive HC. However, potential serious complications should be considered in the application of TAA.

Improvement in exercise capacity and exercise blood pressure response after transcoronary alcohol ablation therapy of septal hypertrophy in hypertrophic cardiomyopathy

Transcoronary alcohol ablation (TAA) therapy of septal hypertrophy was recently proposed as a therapeutic modality for obstructive hypertrophic cardiomyopathy (HC). However, questions remain about the effect of TAA on exercise performance. We performed a time-course analysis of exercise capacity and exercise hemodynamics in 20 patients with symptomatic obstructive HC after TAA. Symptom-limited bicycle exercise testing was performed before and 3 and 12 months after TAA, and cardiac catheterization at 3-month follow-up. The pressure gradient of the left ventricular outflow tract immediately decreased from 58 +/- 8 to 4 +/- 1 mm Hg at rest (p <0.01) and from 143 +/- 11 to 30 +/- 6 mm Hg after extrasystole (p <0.01), but partially recovered at 3-month follow-up (14 +/- 4 and 40 +/- 9 mm Hg, respectively). Left ventricular end-diastolic pressure was not changed after TAA. Peak oxygen consumption increased from 19 +/- 2 to 23 +/- 1 ml/kg/min (p < 0.01) and exercise duration from 573 +/- 47 to 742 +/- 46 seconds (p <0.01) at 3-month follow-up, but thereafter reached a plateau. Abnormal patterns of exercise blood pressure response were shown in 9 patients but normalized after TAA. Major complications occurred in 4 patients: no reflow to the left anterior descending coronary artery in 2 patients and ventricular tachycardia requiring cardioversion in 2 patients. During the follow-up period, all patients survived with symptomatic improvement in 17 patients. Thus, TAA is a promising therapeutic modality with improvement in exercise capacity and abnormal exercise blood pressure response in obstructive HC. However, potential serious complications should be considered in the application of TAA.

Assessing prognosis after acute myocardial infarction in the thrombolytic era.

The use of physiologic testing for prognostication continues to be useful and widely applied in the predischarge evaluation of patients recovering from an uncomplicated acute myocardial infarction in the thrombolytic era. Because patients with abnormal exercise test results are now routinely sent for angiography, there are no randomized trials or experimental confirmation that exercise parameters are still associated with the same prognostic value in the thrombolytic era. Nevertheless, the excellent outcomes in patients treated with thrombolytic therapy and risk stratified with exercise testing provide strong empiric support for the continued use of noninvasive testing of patients without complications after thrombolytic therapy. Reviews of patient cohorts enrolled in trials of thrombolytic therapy show that these patients have a lower incidence of multivessel disease and less evidence of ischemia (ST segment depression or thallium 201 redistribution) compared with prethrombolytic cohorts. For this and other reasons, the sensitivity and specificity of exercise variables for prognosis or detection of multivessel disease are not as strong. The addition of perfusion imaging will enhance the sensitivity for detection of ischemia within or remote from the infarct zone and will provide information regarding viability. Patients who are unable to exercise or those with poor exercise tolerance, an abnormal exercise blood pressure response, inducible ischemia, or nonsustained ventricular tachycardia are candidates for further invasive evaluation and consideration for coronary revascularization. With 201Tl imaging, evidence for increased pulmonary uptake of the tracer is indicative of high risk and a high probability of an adverse outcome with medical therapy. Low-risk patients are those who achieve their target heart rate or work load without inducible angina, ST segment depression, reversible perfusion abnormalities, or increased lung 201Tl uptake. Defect size is reflective of infarct size, and patients with extensive areas of nonreversible hypoperfusion are also at high risk for future events even in the absence of ischemia. Finally, pharmacologic stress imaging with dipyridamole, adenosine, or dobutamine has been found to be safe when employed for stress testing soon after uncomplicated infarction.

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)

Submaximal exercise testing early after myocardial infarction. Difficulty of predicting coronary anatomy and left ventricular performance.

Impaired left ventricular function and extensive coronary artery disease are important determinants of prognosis after acute myocardial infarction. The ability of clinical and predischarge submaximal exercise test variables to predict multivessel coronary artery disease and impaired left ventricular function was assessed in 62 survivors of acute myocardial infarction. Abnormal exercise blood pressure response and short exercise performance were predictors of multivessel disease, but exercise induced ST segment changes and clinical variables were not. Q wave infarction, high grade Killip classification, and exercise induced ST segment elevation predicted statistically significant impairment of resting left ventricular function, whereas other clinical and exercise test variables did not. Exercise induced ST segment changes were therefore of little value in detecting extensive coronary disease, although exercise induced ST elevation was an indicator of poor resting left ventricular function. Although abnormal exercise haemodynamics may detect extensive coronary artery disease, other physiological markers of reversible myocardial ischaemia are probably necessary to plan optimal management in these patients.

Functional and anatomic correlates of markedly abnormal stress tests

The functional state and coronary anatomy of 120 patients evaluated primarily because of a markedly positive ischemic exercise stress test (greater than 2 mm ST depression) is presented. Twenty-seven patients were asymptomatic (group A), 36 patients (group B) had type I angina (Canadian classification) and 57 patients (group C) had angina with only minor limitations (type II angina). All patients underwent exercise stress testing (Bruce protocol) within 2 months of cardiac catheterization. No significant intergroup differences were observed in exercise variables including time of onset of ischemia, maximal heart rate achieved, rate-pressure product, duration of exercise or mean change in blood pressure. Two patients in group A had normal coronary arteriograms. Comparison of the remaining asymptomatic patients in group A with patients in groups B and C revealed no significant differences in the number of coronary arteries involved, main left coronary artery disease, coronary score or the frequency of collateral circulation. In group A, 18% of collateral vessels were in jeopardy compared with 52% in groups B and C (p less than 0.05). Triple vessel disease was present in 57% and left main coronary artery disease in 16% of the total group. The only exercise variable useful in identifying patients with severe coronary disease was an abnormal exercise blood pressure response. This study indicates that a markedly ischemic stress test, regardless of the functional state of the patient, identifies patients, including those without symptoms, who have severe coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)