Comparing Intraocular Pressure, Ocular Blood Flow, and Retinal Nerve Fiber Layer Thickness in Early and Chronic Hypertensives With Normotensives.

PURPOSE: To compare blood pressure (BP), intraocular pressure (IOP), ophthalmic artery flow (OAF) velocity, retinal nerve fiber layer (RNFL) thickness, and visual fields in newly diagnosed hypertension (HT) patients (before treatment), chronic HT (on antihypertensive medications >5 years) and normotensives. METHODS: A prospective, cross-sectional study at a tertiary care centre in India. Three groups of 45 patients each: group 1 - early HT, group 2 - chronic HT, and Group 3 - normotensives, underwent evaluation of BP, IOP by Goldmann applanation tonometry (GAT), OAF velocity by transcranial doppler (TCD), RNFL analysis by spectral-domain optical coherence tomography (SD-OCT), and visual fields. RESULTS: The BP was highest in early HT > chronic HT > normotensives (p < 0.001). The IOP of early HT, chronic HT, and normotensives were 15.87 ± 2.19 mmHg, 13.47 ± 1.92 mmHg, and 15.67 ± SD 1.75 mmHg (p < 0.001). The OAF velocity [peak systolic velocity (PSV), end-diastolic velocity (EDV) in cm/sec] was lowest in chronic HT (30.80 ± 7.05, 8.58 ± 1.58) < early HT (35.47 ± 5.34, 10.02 ± 1.74) < normotensives (36.29 ± 4.43, 10.44 ± 2.29), (p < 0.001). The average RNFL thickness was significantly lower in chronic HT (p = 0.022). The PSV, EDV, and MFV showed significant correlation with IOP (r = 0.247, p = 0.004; r = 0.206, p = 0.016; r = 0.266, p = 0.002) and average RNFL thickness (r = 0.309, p= <0.001; r = 0.277, p = 0.001; r = 0.341, p < 0.001). CONCLUSIONS: Patients with chronic HT demonstrated the lowest retrobulbar flows, IOP and lower RNFL measurements. Lower ocular perfusion may be associated with lower IOP and may be a risk factor for end-organ damage (RNFL) independent of IOP.

Comparing Peribulbar and Topical Anesthesia in Cataract Surgery among Patients with Cardiovascular Disease.

PURPOSE: To compare topical and peribulbar anesthesia in cataract surgery for hemodynamic changes, rate of complications and pain score in patients with cardiovascular disease. METHODS: A prospective comparative study at a tertiary care center in India. Patients >40 years old with treated/controlled hypertension and cardiovascular disease scheduled for cataract surgery under topical or peribulbar anesthesia were recruited. Heart rate, blood pressure, and ophthalmic and systemic complications were noted: preoperatively, immediately after block, intraoperatively, immediately postoperatively and 1 hour postoperatively. A visual analog scale was used to assess the pain score. RESULTS: A total of 150 patients (75 in each group) underwent cataract surgery. There was a significant rise in pulse rate and blood pressure after peribulbar injection and intraoperatively, which gradually reduced to baseline 1 hour after surgery in both groups (p < 0.001), with systolic blood pressure intraoperatively being significantly greater in the peribulbar group (155.49 ±18.14 mmHg vs. 147.95 ±17.71 mmHg, p = 0.01). The topical group had slightly lower visual analog scale scores (1.12 ± 0.99) than the peribulbar group (1.44 ± 0.90, p = 0.04). CONCLUSIONS: Cataract surgery appears safe in patients with adequately controlled cardiovascular disease, and topical anesthesia may be preferable due to noninvasiveness, adequate analgesia, and minimal effect on hemodynamic parameters. Therefore, hemodynamically stable patients of cardiovascular disease undergoing uncomplicated cataract surgery may be counselled for topical anesthesia.

Effect of Blood Pressure Reduction on Intraocular Pressure and Ophthalmic Artery Blood Flow Velocity in Hypertension.

Purpose: To evaluate the effect of reducing blood pressure (BP) by atenolol and amlodipine on (1) intraocular pressure (IOP) and (2) ophthalmic artery blood flow (OAF) velocity in new hypertensives. Methods: A prospective, observational cohort study conducted at a tertiary care center in India after IRB approval. New hypertensives treated with atenolol 25 mg or amlodipine 5 mg were divided into 2 groups of 30 patients each. BP, IOP by Goldmann applanation tonometry and OAF velocity by transcranial doppler sonography was performed before medication and post medication on day 1, 7, and 30. Results: There was a significant decrease in IOP with both drugs; the effect was greater with atenolol. Atenolol: premedication IOP - 16.06 ± 2.13 mmHg and day 30-12.46 ± 1.94 (22.4%) [P < 0.001], amlodipine: premedication IOP-15.13 ± 2.55 mmHg and day 30- 13.06 ± 2.14 (13.68%) [P < 0.001]. A decrease of 0.5 mmHg in IOP with every 10 mmHg (95% CI: 0.121-0.826, P value = 0.01) decrease in systolic BP was noted after oral atenolol. The OAF peak systolic velocity and mean flow velocity were equally reduced with both drugs (P < 0.001). The end-diastolic velocity, reduced only with atenolol (P = 0.049) but returned to baseline with amlodipine at 1 month. Conclusions: BP reduction by atenolol and amlodipine led to decreases in IOP and OAF velocity, greater with atenolol. The IOP decrease was likely due to reduced blood flow. A slight decrease in the diastolic flow of the ophthalmic artery was noted with atenolol.

Body surface distribution of T wave alternans is modulated by heart rate and ventricular activation sequence in patients with cardiomyopathy.

BACKGROUND: T wave alternans (TWA) is an electrocardiographic marker of heightened sudden death risk from ventricular tachyarrhythmias in patients with cardiomyopathy. TWA is evaluated from the 12-lead electrocardiogram, Frank lead, or Holter lead recordings, however these clinical lead configurations will not record TWA from adjacent regions of the body torso. OBJECTIVE: We tested the hypothesis that changing heart rate or ventricular activation may alter the body surface distribution of TWA such that the clinical ECG leads fail to detect TWA in some patients; thereby producing a false-negative test. METHODS: In 28 cardiomyopathy patients (left ventricular ejection fraction 28±6%), 114 unipolar electrograms were recorded across the body torso during incremental atrial pacing, followed by atrioventricular pacing at 100, 110 and 120bpm. TWA was measured from each unipolar electrogram using the spectral method. A clinically positive TWA test was defined as TWA magnitude (Valt) ≥1.9 uV with k ≥3 at ≤110bpm. RESULTS: Maximum Valt (TWAmax) was greater from the body torso than clinical leads during atrial (p<0.005) and atrioventricular pacing (p<0.005). TWAmax was most prevalent in the right lower chest with atrial pacing 100 bpm and shifted to the left lower chest at 120 bpm. TWAmax was most prevalent in left lower chest with atrioventricular pacing at 100 bpm and shifted to the left upper chest at 120 bpm. Using the body torso as a gold standard, the false-negative rate for clinically positive TWA with clinical leads was 21% during atrial and 11% during atrioventricular pacing. Due to TWA signal migration outside the clinical leads, clinically positive TWA became false-negative when pacing mode was switched (atrial→atrioventricular pacing) in 21% of patients. CONCLUSIONS: The body surface distribution of TWA is modulated by heart rate and the sequence of ventricular activation in patients with cardiomyopathy, which can give rise to modest false-negative TWA signal detection using standard clinical leads.

Combined ST Elevation in a Case of Acute Myocardial Infarction: How to Identify the Infarct-related Artery?

Combined ST elevation in anterior and inferior ECG leads in acute myocardial infarction is not a rarity. It is both interesting and challenging to indentify the infarct related culprit artery. We report the case of a middle aged male with acute myocardial infarction whose admission ECG shows ST elevation in lead II, III, aVF as well as from V1-V3. 90% of such cases are due to single vessel occlusion - majority due to proximal RCA occlusion and the remaining due to mid to distal LAD occlusion. ECG features to differentiate between these two vascular occlusions are discussed. In this case at hand, lead III ST elevation of 2.5 mm and V2/V3≥ 1 indicates proximal RCA as the IRA and the same has been confirmed by pre-discharge coronary angiogram .

Bidirectional ventricular tachycardia of unusual etiology.

Bidirectional ventricular tachycardia (BDVT) is a rare form of ventricular arrhythmia, characterized by changing QRS axis of 180 degrees. Digitalis toxicity is considered as commonest cause of BDVT; other causes include aconite toxicity, myocarditis, myocardial infarction, metastatic cardiac tumour and cardiac channelopathies. We describe a case of BDVT in a patient with Anderson-Tawil syndrome.

A dangerous twist of the 'T' wave: A case of Wellens' Syndrome.

Wellens' syndrome is a condition in which electrocardiographic (ECG) changes indicate critical proximal left anterior descending artery narrowing occurring during the chest pain-free period. Due to the severity of the obstruction, if such cases are managed by early invasive revascularisation therapy, a major threat in the form of a massive myocardial infarction or sudden death may be averted. We present the case of a patient with previous chest pain, whose ECG showing subtle ischemic changes was initially overlooked. A repeat ECG taken during the painless period showed a biphasic T wave, suggestive of Wellen's' syndrome. This was confirmed by an immediate coronary angiogram.

Ventricular Tachycardia Precipitated by Short-long-short Sequence in a Patient with Implantable-cardioverter Defibrillator.

Abrupt changes in heart rate, particularly short-long-short sequences in the ventricular cycle length (CL), might precede initiation of ventricular tachycardia/fibrillation (VT/VF). These changes may be facilitated or caused by pacing activity in patients with pacemakers or implantable-cardioverter defibrillators (ICDs). We describe a patient with two episodes of acquired VT precipitated by short-long-short sequences and diagnosed from the ICD recordings. In such cases, the knowledge of the device parameters is extremely important for a correct diagnosis and management.

Modulated dispersion of activation and repolarization by premature beats in patients with cardiomyopathy at risk of sudden death.

Premature beats can trigger ventricular arrhythmias in heart disease, but the mechanisms are not well defined. We studied the effect of premature beats on activation and repolarization dispersion in seven patients with cardiomyopathy (57 ± 10 yr, left ventricular ejection fraction 31 ± 7%). Activation time (AT), activation-recovery interval (ARI), and total repolarization time (TRT) were measured from 26 unipolar electrograms during right ventricle (RV) endocardial (early) to left ventricle epicardial (late) activation in response to RV apical extrastimulation (S1S2). Early TRT dispersion increased significantly with shorter S1S2 (1.0 ± 0.2 to 2.3 ± 0.4 ms/mm, P < 0.0001), with minimal change in late TRT dispersion (0.8 ± 0.1 to 1.0 ± 0.3 ms, P = 0.02). This was associated with an increase in early AT dispersion (1.0 ± 0.1 to 1.5 ± 0.2 ms/mm, P = 0.05) but no change in late AT dispersion (0.6 ± 0.1 to 0.7 ± 0.2 ms/mm, P = 0.4). Early and late ARI dispersion did not change with shorter S1S2. AT restitution slopes were similar between early and late sites, as was slope heterogeneity. ARI restitution slope was greater in early vs. late sites (1.3 ± 0.6 vs. 0.8 ± 0.6, P = 0.03), but slope heterogeneity was similar. With shorter S1S2, AT-ARI slopes became less negative (flattened) at both early (-0.4 ± 0.1 to +0.04 ± 0.2) and late (-1.5 ± 0.2 to +0.3 ± 0.2) sites, implying less activation-repolarization coupling. There was no difference in AT-ARI slopes between early and late sites at short S1S2. In conclusion, high-risk patients with cardiomyopathy have greater TRT dispersion at tightly coupled S1S2 due to greater AT dispersion and activation-repolarization uncoupling. Modulated dispersion is more pronounced at early vs. late activated sites, which may predispose to reentrant ventricular arrhythmias.