Arun J Baksi

A Meta-Analysis of the Mechanism of Blood Pressure Change With Aging

OBJECTIVESnWe undertook a meta-analysis to determine whether changes in wave reflection substantiate the consensus explanation of why blood pressure (BP) changes with aging.nnnBACKGROUNDnConsensus documents attribute the aging changes in BP to wave reflection moving progressively from diastole into systole. However, the extensive quantitative data on this phenomenon have never been systematically reviewed. Individual studies have been small, and limited to a narrow age range.nnnMETHODSnUsing PubMed, Cochrane, and Web of Science databases, we identified 64 studies (including 13,770 subjects, age range 4 to 91 years) reporting the timing of wave reflection, defined as the time from the onset (foot) of the pressure waveform to the shoulder point (anachrotic notch).nnnRESULTSnIn subjects of all ages, reflection times were well within systole. There was a small tendency for younger subjects to have later reflection, but this was only 0.7 ms per year, whereas the weighted mean reflection time was 136 ms (99% confidence interval: 130 to 141 ms) and the mean duration of systole was 328 ms (99% confidence interval: 310 to 347 ms). At this rate of change with age, arrival of wave reflection would only be construed to be in diastole at an extrapolated age of -221 years.nnnCONCLUSIONSnThese findings challenge the current consensus view that a shift in timing of wave reflection significantly contributes to the changes in the BP waveform with aging. We should re-evaluate the mechanisms of BP elevation in aging.

T2* imaging of the heart: methods, applications, and outcomes.

Abstract This review describes and discusses the rationale, technique, applications, and impact of cardiovascular magnetic resonance (CMR) T2* imaging, principally in the assessment of iron loading within the heart, and highlights how this robust imaging strategy has transformed disease outcome. Until recently, no simple noninvasive measurement was available to reliably indicate severe cardiac iron loading before the development of overt cardiac dysfunction or heart failure. Consequently, the majority of patients with transfusion-dependent anemias, such as &bgr;-thalassemia major, died prematurely of cardiovascular complications of severe iron overload. The magnetic properties of particulate iron disrupt magnetic field homogeneity in the CMR environment and consequently influence the CMR parameter T2*, which describes signal decay relating to both field inhomogeneity and loss of spin coherence. There is a direct relationship between T2* and myocardial iron concentration, enabling this to be used to identify and quantify myocardial iron load. Single breath-hold gradient-echo sequences in which a single midventricular short-axis myocardial slice is acquired at multiple echo times enables a myocardial T2* value to be measured from the rate of exponential decay. The application of T2* CMR to assessing cardiac iron loading is rapid, reproducible, extensively validated, and now widely performed. Data have highlighted the profound predictive power of this imaging technique and moreover its ability to inform management strategies such that, over a relatively short duration, outcome has been dramatically improved, and the disease course in &bgr;-thalassemia major transformed.

Long-Term Antihypertensive Treatment Fails to Improve E/e′ Despite Regression of Left Ventricular Mass: An Anglo-Scandinavian Cardiac Outcomes Trial Substudy

Antihypertensive treatment can improve tissue Doppler indices of left ventricular diastolic function in the short term, but little is known about the longer-term effect of different antihypertensive treatments on progression of left ventricular diastolic function and left ventricular hypertrophy. We hypothesized that long-term treatment of hypertension will lead to improvements in left ventricular hypertrophy and diastolic function. We collected detailed cardiovascular phenotypic data on 1006 participants from a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial. Patients randomized to either an amlodipine±perindopril-based or an atenolol±bendroflumethiazide-based regimen underwent conventional and tissue Doppler echocardiography at time of control of blood pressure after randomization (≈1.5 years; phase 1) and after a further 2 years of antihypertensive treatment (phase 2). There were no prerandomization data. Five hundred thirty-six patients had complete data collection at both phases. Left ventricular mass index regressed from phase 1 to 2 with no significant difference between treatment groups (amlodipine: 119.5–116.8; atenolol: 122.9–117.5; P<0.001 for both). Conversely, tissue Doppler diastolic indices did not change in the amlodipine±perindopril-based regimen (E/e′, 7.5–7.6 cm/s; P=not significant), but deteriorated in the atenolol±bendroflumethiazide-based regimen (E/e′, 8.0–8.5 cm/s; P<0.01). Despite regression of left ventricular hypertrophy, there was no associated improvement in diastolic function. In fact, long-term treatment with atenolol±bendroflumethiazide resulted in a progressive deterioration in E/e′. This may be a factor contributing to the previously described worse clinical outcome in patients treated with atenolol±bendroflumethiazide compared with amlodipine±perindopril.

Prognostic significance of ventricular function and late gadolinium enhancement on CMR in symptomatic patients with scleroderma

Background Cardiac involvement is a leading cause of morbidity and premature mortality in patients with scleroderma. Identification of this offers the opportunity for earlier and more stratified therapeutic intervention. Published data on the prognostic significance of left and right ventricular impairment and myocardial fibrosis in this cohort are limited. The study objective was to determine the prevalence and prognostic significance of abnormalities on cardiovascular magnetic resonance (CMR) in patients with scleroderma who have breathlessness and/or other cardiac symptoms. Methods This is a retrospective longitudinal study of 126 consecutive patients with confirmed scleroderma and cardiac symptoms, who had undergone CMR. Completed scans were available in 124 of these. All scans were performed at 1.5 Tesla (Siemens Sonata or Avanto). Thinned myocardium was defined as thickness 5mm. The presence of left ventricular (LV) or right ventricular (RV) dilatation was defined as an increase in indexed LV or RV volumes compared to previously published normal ranges. Late gadolinium enhancement (LGE) was defined as an area of clearly increased signal intensity confirmed on phase swapping. All scans were analysed by two independent operators. All cause mortality was determined from review of hospital records and the national summary care database. A Cox proportional hazards model was used to determine predictors of mortality (IBM SPSS 19, USA). Results Demographic data and CMR findings are shown in Table 1. Mean age was 55 (range 19 to 82) years, 45% were male and 81% had at least one cardiovascular abnormality on the scan. Significant LV dysfunction (ejection fraction<45%) was evident in 12% of patients and reduction in RV ejection fraction in 20% of patients. Myocardial fibrosis by LGE was found in 21% of patients (Table 1). The number of patients with 1, 2 or 3 cardiovascular abnormalities on CMR were 13%, 13% and 10% respectively. In total, 46% of the patients had 4 or more abnormalities. There were 21 deaths during the follow-up period. CMR predictors of mortality were LV ejection fraction<45% (Hazard ratio [HR] 3.9, 95% confidence interval [CI] 1.52-9.84, P=0.004) and impaired RV ejection fraction (HR 2.6, 95%CI 1.04-6.38, P=0.04). The presence of LGE did not predict mortality (HR 1.05, 95%CI 0.34-3.16, P=0.94).

Use of contrast enhanced magnetic resonance angiography in assessment of anatomic suitability for renal denervation in the hypertensive population

Background Renal denervation (RDN) is an effective treatment for resistant hypertension with expanding indications in the hypertensive population [1]. The European Society of Hypertension (ESH) guidelines [2], largely based on the Symplicity trial inclusion criteria, state RDN should not be performed if the patient has multiple renal arteries, renal artery stenosis or renal arteries with a diameter of less than 4 mm or length of less than 20 mm. Imaging prior to consideration of RDN is recommended but has not been included in all RDN trial protocols. The proportion of hypertensive patients with anatomy suitable for RDN using the current guidelines is not known.

The association between ECV and microcirculation perfusion abnormalities in non-ischemic dilated cardiomyopathy

Background Myocardial fibrosis and abnormalities of the microcirculation are features of non-ischemic dilated cardiomyopathy (DCM) and may contribute to adverse remodeling. However, relationship between perfusion abnormalities and diffuse fibrosis has not been fully characterised. CMR allows quantification of the extracellular volume fraction (ECV), a marker of fibrosis, and absolute myocardial blood flow, in a single study. We hypothesised that increased ECV was associated with impaired myocardial perfusion reserve (MPR) in DCM patients. Methods

Long-Term Antihypertensive Treatment Fails to Improve E/e′ Despite Regression of Left Ventricular MassNovelty and Significance

Antihypertensive treatment can improve tissue Doppler indices of left ventricular diastolic function in the short term, but little is known about the longer-term effect of different antihypertensive treatments on progression of left ventricular diastolic function and left ventricular hypertrophy. We hypothesized that long-term treatment of hypertension will lead to improvements in left ventricular hypertrophy and diastolic function. We collected detailed cardiovascular phenotypic data on 1006 participants from a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial. Patients randomized to either an amlodipine±perindopril-based or an atenolol±bendroflumethiazide-based regimen underwent conventional and tissue Doppler echocardiography at time of control of blood pressure after randomization (≈1.5 years; phase 1) and after a further 2 years of antihypertensive treatment (phase 2). There were no prerandomization data. Five hundred thirty-six patients had complete data collection at both phases. Left ventricular mass index regressed from phase 1 to 2 with no significant difference between treatment groups (amlodipine: 119.5–116.8; atenolol: 122.9–117.5; P<0.001 for both). Conversely, tissue Doppler diastolic indices did not change in the amlodipine±perindopril-based regimen (E/e′, 7.5–7.6 cm/s; P=not significant), but deteriorated in the atenolol±bendroflumethiazide-based regimen (E/e′, 8.0–8.5 cm/s; P<0.01). Despite regression of left ventricular hypertrophy, there was no associated improvement in diastolic function. In fact, long-term treatment with atenolol±bendroflumethiazide resulted in a progressive deterioration in E/e′. This may be a factor contributing to the previously described worse clinical outcome in patients treated with atenolol±bendroflumethiazide compared with amlodipine±perindopril.

Long-Term Antihypertensive Treatment Fails to Improve E/e′ Despite Regression of Left Ventricular MassNovelty and Significance: An Anglo-Scandinavian Cardiac Outcomes Trial Substudy

Antihypertensive treatment can improve tissue Doppler indices of left ventricular diastolic function in the short term, but little is known about the longer-term effect of different antihypertensive treatments on progression of left ventricular diastolic function and left ventricular hypertrophy. We hypothesized that long-term treatment of hypertension will lead to improvements in left ventricular hypertrophy and diastolic function. We collected detailed cardiovascular phenotypic data on 1006 participants from a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial. Patients randomized to either an amlodipine±perindopril-based or an atenolol±bendroflumethiazide-based regimen underwent conventional and tissue Doppler echocardiography at time of control of blood pressure after randomization (≈1.5 years; phase 1) and after a further 2 years of antihypertensive treatment (phase 2). There were no prerandomization data. Five hundred thirty-six patients had complete data collection at both phases. Left ventricular mass index regressed from phase 1 to 2 with no significant difference between treatment groups (amlodipine: 119.5–116.8; atenolol: 122.9–117.5; P<0.001 for both). Conversely, tissue Doppler diastolic indices did not change in the amlodipine±perindopril-based regimen (E/e′, 7.5–7.6 cm/s; P=not significant), but deteriorated in the atenolol±bendroflumethiazide-based regimen (E/e′, 8.0–8.5 cm/s; P<0.01). Despite regression of left ventricular hypertrophy, there was no associated improvement in diastolic function. In fact, long-term treatment with atenolol±bendroflumethiazide resulted in a progressive deterioration in E/e′. This may be a factor contributing to the previously described worse clinical outcome in patients treated with atenolol±bendroflumethiazide compared with amlodipine±perindopril.

Cardiac magnetic resonance perfusion imaging and the effects of single intravenous cannulation with the Octopus bionector

Background CMR perfusion (CMRP) imaging using adenosine traditionally requires bilateral arm cannulation. Patients with multiple comorbidities often have difficult venous access and dual cannulation often proves impossible. We used a standard two-way adapter (Octopus Vygon with no-reflow valve) to administer adenosine at a standard rate of 140 mcg/kg/minute over 3 minutes for maximum coronary vasodilatation following a bolus injection of gadolinium. High flow bolus injection may cause sinus arrest caused by a flush of residual adenosine in the same arm vein. We acquired 50 sequential R-wave triggered image frames to assess first pass myocardial perfusion and assessed the effect of significant sinus pauses on image acquisition.

Cine acquisition strategies for visualizing atrial septal defects by CMR

Background Atrial septal defects (ASDs) may escape detection before adulthood, particularly those in unusual locations, which may elude echocardiographic visualisation. CMR is established for the quantification of shunt flow and, if appropriately acquired, can provide clear visualisation of ASDs and adjacent structures to inform decisions regarding intervention. Our objective is to recommend cardiovascular magnetic resonance (CMR) cine acquisition strategies suitable for the visualisation of the less common as well as the common types of ASD. Methods In the CMR Unit of a tertiary referral centre for adults with congenital heart disease we retrospectively reviewed the CMRs of patients with unoperated ASDs over a 3 year period to assess the suitability of cine acquisition strategies for the visualisation of different types of ASD and any associated anomalies of pulmonary venous connection. Results 157 patients with unoperated ASDs had CMR studies in 3 years. If already suspected, we had routinely acquired an ‘atrial stack’ of cines, meaning a contiguous stack, 5mm thick, parallel to the routine ventricular short axis (SA) stack, stepping backward from the basal ventricular plane until the superior vena cava was identifiable. This orientation visualized ostium secundum ASDs well (n=117), and was also good for inferior sinus venosus defects (n=2) and unroofed coronary sinus (n=3). In superior sinus venosus defects (n=21), a transaxial cine stack was found to give clearer visualisation of both the defect and any associated anomalous pulmonary vein connection(s) (n=20, plus 4 anomalous connections identified with secundum ASDs). The transaxial cine orientation was also the more suitable one for atrio-ventricular septal defects (AVSD, n=15) as it depicted insertions of the A-V valve leaflets adjacent to the defect(s). Conclusions In patients with suspected ASDs, we recommend the acquisition of an atrial SA cine stack and a transaxial cine stack that covers atrial to aortic arch levels. Additional oblique cines aligned with the defect can supplement these, as indicated in the table. Funding None.