Mark Dancy

MISDIAGNOSIS OF CHRONIC RECURRENT VENTRICULAR TACHYCARDIA

24 patients with recurrent ventricular tachycardia were repeatedly misdiagnosed as having supraventricular tachycardia. Supraventricular tachycardia was recorded as the diagnosis 163 times in these patients. 72 12-lead electrocardiograms (ECGs) were available and they were reviewed together with the notes made at the time of the ECGs to discover the reasons for misdiagnosis. 7 consultant cardiologists, 22 consultant physicians, 13 senior registrars, and 57 registrars were involved in the misdiagnosis. Retrospective application of the established criteria used to distinguish ventricular tachycardia from supraventricular tachycardia with aberrancy enabled the diagnosis of ventricular tachycardia to be made in 22/24 patients (92%). In all but 2/72 episodes the only differentiating criterion noted by the attending physicians was dissociated atrial activity, and there seemed to be considerable bias in favour of the diagnosis of supraventricular tachycardia. 20/24 patients were given inappropriate treatment, which had dangerous consequences in 5.

PRECLINICAL LEFT VENTRICULAR ABNORMALITIES IN ALCOHOLICS ARE INDEPENDENT OF NUTRITIONAL STATUS, CIRRHOSIS, AND CIGARETTE SMOKING

M mode echo recordings of the left ventricle (LV) were performed in 33 patients with alcoholic liver disease, 26 patients with various non-alcoholic liver diseases, and in 18 non-alcoholic controls. Groups were well matched for age and overall nutritional status (as assessed by anthropometry) and none of the subjects studied had cardiorespiratory symptoms. Alcoholics had significantly increased LV free wall thickness and LV cavity dimension at end diastole (EDD). Multiple regression analysis of the data identified alcohol abuse as the most important variable affecting EDD, and this relation could not be explained by differences in age, sex, overall nutrition, cigarette smoking, thiamine status (total blood thiamine and thiamine pyrophosphate concentration), presence of liver disease, or severity of liver disease (cirrhotic vs non-cirrhotic). The increase in LV free wall thickness was not significantly related to alcohol abuse. These results suggest that chronic alcohol abuse is an important independent risk factor for cardiac dilatation, and that increase in EDD may be an early marker of alcoholic cardiomyopathy.

Age-associated changes in left ventricular diastolic function are related to increasing left ventricular mass

Isometric exercise (IME) produces significant hemodynamic changes in the cardiovascular system. We have used IME to study the effect of age on diastolic left ventricular (LV) function in 100 normal volunteers. The E/A ratio (peak velocity of early/atrial filling phases), deceleration time (DT), and isovolumic relaxation time (IVRT) of the transmitral flow were assessed during echocardiography with pulsed-Doppler ultrasound at rest and at peak IME using handgrip. LV mass index (LVMI) and LV ejection fraction (LVEF) were also calculated. Both E/A and IVRT reduced significantly with increasing age. The LVEF decreased (P <.0001), whereas LVMI increased (P <.05) with advancing age. The LVEF was inversely related to LVMI (P <.05). An inverse relationship was noted between E/A and LVMI (P <.01) during IME. The contribution of the atrial contraction to the total diastolic flow increased significantly with advancing age (P <.02) and increased from 0.29 +/- 0.04 at rest to 0.34 +/- 0.08 during IME (P <.0001). It is concluded that with progressing age, the left ventricle becomes stiffer resulting in a reduction in early filling and a compensatory increase in flow due to atrial contraction. A progressive increase in LVMI, which accompanies aging may contribute to stiffening of the left ventricle and deterioration in diastolic function of the left ventricle. This is exaggerated by IME.

Blood thiamine and thiamine phosphate ester concentrations in alcoholic and non-alcoholic liver diseases.

Thiamine state was investigated in patients with alcoholic liver disease, patients with various non-alcoholic liver diseases, and controls using a direct technique (thiochrome assay) to measure thiamine, thiamine monophospate, and the active coenzyme thiamine pyrophosphate in whole blood after isolating the fractions by ion exchange chromatography. Overall nutrition was similar in all groups as assessed by anthropometry, and no patient had clinical evidence of thiamine deficiency. There was no significant difference among the groups in mean concentration of any form of thiamine. The scatter was much greater in patients with alcoholic liver disease but only 8.7% had biochemical thiamine deficiency (defined as a blood concentration of the active coenzyme greater than 2 SD below the mean control value). An unexpected finding was of abnormally high total thiamine concentrations (greater than 2 SD above the mean control value) in 17.4% of patients with alcoholic liver disease, the highest concentrations being found in two patients with severe alcoholic hepatitis and cirrhosis. The ratio of phosphorylated to unphosphorylated thiamine was calculated as an index of phosphorylation and, although the mean did not differ significantly among the groups, the range was greatest in alcoholic liver disease. The lowest ratios occurred in the two patients with severe alcoholic hepatitis, but neither had evidence of thiamine pyrophosphate deficiency. Contrary to studies using indirect assay techniques, these results suggest that thiamine deficiency is unusual in well nourished patients with alcoholic liver disease. The new finding of unexpectedly high thiamine concentrations in some patients may be due to abnormalities of hepatic storage or release in liver disease, particularly in severe alcoholic hepatitis. There was no convincing evidence of impaired thiamine phosphorylation in any patients with liver disease. Conclusions from studies using indirect assays on the prevalence and mechanisms of thiamine deficiency in liver diseases may not be valid.

Significance of complete right bundle-branch block when an isolated finding. An echocardiographic study.

Twenty-seven patients with complete right bundle-branch block as the only abnormal finding were studied using high speed M-mode echocardiography to determine the effect of the electrical delay on the mechanical events of right ventricular systole. Pulmonary valve opening (PVOm) was delayed in all cases. In some the delay was mainly between mitral valve closure (MVC) and tricuspid valve closure (TVC), and this was designated proximal block. In the others the main delay was between tricuspid valve closure and pulmonary valve opening and this was designated distal block. The patients were divided into those with proximal and those with distal block by calculating the ratio TVC-PVOm/MVC-TVC. Twelve out of 13 of those with distal delay but only one out of 14 of those with proximal delay had episodes of syncope or near syncope. These results are consistent with previous theories about the pathophysiology of right bundle-branch block. Echocardiography may offer a non-invasive method to estimate the prognosis in isolated right bundle-branch block.

Balloon dilatation of the aortic valve: limited success and early restenosis.

Balloon dilatation of the aortic valve was attempted 16 times in 15 patients with severe aortic stenosis. None died but one had a transient stroke after the procedure. At dilatation the gradient across the aortic valve was reduced by greater than 30% in 69% of patients and the Gorlin valve area (calculated in 7/15 patients) increased by 30% in half. But a comparison of Doppler gradients measured before and one to two days after dilatation in 11 patients showed a greater than 30% reduction in the simultaneously measured gradient in only four. Doppler gradient was the most accurate predictor of symptomatic benefit and a fall in Doppler gradient persisted mainly in patients whose peak to peak gradient fell by at least 40% at the time of the procedure. Balloon dilatation of the aortic valve is a relatively safe procedure but it is less successful than previous reports suggest, perhaps because of early restenosis. Some forms of aortic stenosis may be more amenable to this procedure than others.

The Glucose Tolerance Test, But Not HbA 1c, Remains the Gold Standard in Identifying Unrecognized Diabetes Mellitus and Impaired Glucose Tolerance in Hypertensive Subjects

The objective of this study was to compare the value of the oral glucose tolerance test (GTT), glycated hemoglobin concentration (HbA1c), and fasting plasma glucose (FPG) for identifying unrecognized diabetes mellitus (DM) and impaired glucose tolerance (IGT) in hypertensive subjects. One hundred forty-four consecutive subjects who were not known to have DM and who were attending the Hypertension Clinic underwent 24-hour ambulatory blood pressure (BP) monitoring. A GTT and an HbA1c measurement were also carried out. Abnormal results from GTT were found in 94 patients (65%). Results from FPG were not different between those with DM and IGT but were significantly higher than in the euglycemic subjects. The FPG was between 110-125 mg/dL (6.1-6.9 mmol/L) in 31% (n=20) of patients with IGT and in 53% (n=16) of those with DM. With use of the previously published criteria to diagnose DM of FPG ≥103 mg/dL (5.7 mmol/L) and HbA1c ≥5.9%, 33% of our diabetic subjects and 75% of those with IGT would have been misclassified as euglycemic. The previously reported cut-off point for HbA1c of >6.1% to diagnose DM was present in 77% of our patients with DM and in 14% (n=9) of the patients with IGT. Multiple regression analysis showed that an abnormal result from GTT was independent of the level of clinical or ambulatory BP, nocturnal BP dip, cholesterol level, smoking history, race, or class of antihypertensive medication taken. FPG levels or HbA1c, or their combination, are not accurate enough to identify DM or IGT in patients attending a hospital Hypertension Clinic. A GTT may be required in these patients to reliably identify those with DM or IGT.

Right ventricular stunning in inferior myocardial infarction

AIM To assess right ventricular (RV) function in patients with inferior myocardial infarction (IMI) and to observe changes following thrombolysis. BACKGROUND RV dysfunction occurs in 30% of patients with IMI. The extent of such involvement and its potential, recovery has not been determined. METHODS We studied 30 patients with acute IMI (age 56+/-12 years), on admission, day 7 and day 30 post thrombolysis. No patient had clinical signs of RV failure. RV segmental function was assessed from free wall long axis and global function from filling and ejection velocities. Values were compared with 15 age-matched controls. RESULTS On admission, RV long axis amplitude, systolic and diastolic velocities were depressed (2.09+/-0.39 vs 2.6+/-0.3 cm, 8.18+/-1.8 vs 10.0+/-2.0 cm/s and 6.9+/-2.7 vs 10.0+/-2.5 cm/s, p<0.01 for all) and global function impaired; reduced Z ratio (0.85+/-0.07 vs 0.9+/-0.04, p<0.01), raised Tei index (0.49+/-0.26 vs 0.3+/-0.1, p<0.001) and prolonged t-IVT (8.16+/-3.9 vs 4.8+/-2 s/m, p<0.01) compared to controls. After thrombolysis, RV long axis amplitude (2.28+/-0.3 cm, p<0.05), systolic velocity (10.0+/-2.7 cm/s, p<0.01), early diastolic velocity (8.3+/-2.16, p<0.05), Z ratio (0.9+/-0.05, p<0.01), Tei index (0.34+/-0.17, p<0.01) and t-IVT (6.2+/-2.7 s/m, p<0.05) all normalised at day 30. Only 4 (13%) patients remained with RV long axis amplitude and one with t-IVT and Tei index values outside the normal 95% CI at day 30. RV inflow diameter and tricuspid regurgitation did not change. CONCLUSION In IMI, RV segmental and global functions are acutely impaired, and recover in 87% of patients following thrombolysis. In the absence of clear evidence for RV infarction the disturbances in the remaining 13% may represent stunned myocardium that may demonstrate delayed recovery.

Induced ischemia detected by dobutamine stress echocardiography in coronary heart disease patients after myocardial re-vascularization.: Experience in a District General Hospital

Most episodes of myocardial ischemia in patients with known coronary artery disease (CHD) are asymptomatic. Silent myocardial ischemia (SMI) is an important predictor of adverse outcome in patients with proven coronary artery disease. beta-blockers are effective in suppressing ischemia, and improve clinical outcome in patients with coronary artery disease. At present, it is common practice to stop treatment with beta-blockers in clinically asymptomatic patients after coronary artery bypass graft (CABG) and/or myocardial re-vascularization (PTCA/Stent), although the possible presence of SMI/inducible ischemia after myocardial re-vascularization is not known. We examined 56 asymptomatic CHD patients after coronary artery bypass graft (n=36), percutaneous coronary angioplasty PTCA/stent (n=15), or both (n=5); therapy with beta-blockers was stopped in all of them after myocardial revascularization. All these patients underwent a dobutamine stress echocardiography test (DSE test). The DSE test was proposed to these asymptomatic CHD patients to investigate the possible presence of SMI/inducible ischemia after myocardial re-vascularization. All patients had history of myocardial infarction or evidence of mildly impaired left ventricular function at rest as assessed by cardiac catheterization. Abnormal DSE studies occurred in eight of the 56 patients (14%; 95% C.I.: 6-26%). Therapeutic approaches specifically targeted at reducing total ischaemic burden include pharmacologic therapy and myocardial revascularization. On the basis of these data, it can be concluded that asymptomatic CHD patients after myocardial re-vascularization must be re-evaluated to rule out SMI/inducible ischemia that can be treated (e.g. with beta-blockers) reducing cardiovascular morbidity and mortality.

The degree of albuminuria is related to left ventricular hypertrophy in hypertensive diabetics and is associated with abnormal left ventricular filling: A pilot study

The association of albuminuria and left ventricular (LV) hypertrophy (LVH) in diabetics aggra vates the prognosis. The authors studied the relation between LVH and the degree of albu minuria in diabetics and investigated the relationship of albuminuria to LV filling. A comparison was made between 30 hypertensive diabetics, 10 of whom had microalbuminuria (MIC) and 20 had macroalbuminuria (MAC), and 18 diabetics who were normotensive and normalbuminuric (NOR). LV mass index (LVMI) and LV ejection fraction (LVEF) were measured during echocar diography. LV filling pattern at rest and at peak standardized isometric exercise (IME) using handgrip was assessed by measuring E/A (peak velocity of the early/atrial filling waves) of the transmitral flow during Doppler and echocardiography. Each patient underwent a stress ECG test. LVMI was higher in MAC (132.3 ±55.4) than in MIC (115.6 ±32.5) or NOR (90.0 ±31.8) (p<0.01). There were more patients in MAC with LVH (n = 13) and abnormal filling (n = 9 at rest and 16 with IME) than in MIC (LVH = 5, abnormal filling = 1 at rest and 10 during IME) or NOR (LVH = 3, abnormal filling = 1 at rest and 9 during IME) (p < 0.02). LVMI was not related to LVEF. Although blood pressure was not different between MAC and MIC groups, it was signif icantly higher than in the NOR group. This study suggests that a high degree of albuminuria in hypertensive diabetics is associated with greater value for LVMI and an increased incidence of LVH independent of blood pressure level or systolic LV function. LVH is associated with abnormal LV filling. The degree of albuminuria may predict LVMI and LVH, which are associated with abnormal LV filling. This association of abnormal LV filling with albuminuria in hypertensive diabetic patients may account for their high risk of cardiovascular events.