Nagehan Kucukler

Stress induced hypertensive response: should it be evaluated more carefully?

Various diagnostic methods have been used to evaluate hypertensive patients under physical and pharmacological stress. Several studies have shown that exercise hypertension has an independent, adverse impact on outcome; however, other prognostic studies have shown that exercise hypertension is a favorable prognostic indicator and associated with good outcome. Exercise hypertension may be encountered as a warning signal of hypertension at rest and future hypertensive left ventricular hypertrophy. The results of diagnostic stress tests support that hypertensive response to exercise is frequently associated with high rate-pressure product in hypertensives. In addition to the observations on high rate-pressure product and enhanced ventricular contractility in patients with hypertension, evaluation of myocardial contractility by Doppler tissue imaging has shown hyperdynamic myocardial function under pharmacological stress. These recent quantitative data in hypertensives suggest that hyperdynamic myocardial function and high rate-pressure product response to stress may be related to exaggerated hypertension, which may have more importance than that it has been already given in clinical practice.

Quantitative left ventricular contractility analysis under stress: a new practical approach in follow-up of hypertensive patients

Excessive sympathetic activity and stress-induced left ventricular (LV) hypercontractility have been described in hypertensive LV hypertrophy. Recent quantitative data have shown that hypertensive LV hypertrophy is associated with preserved global LV function. However, progression of uncontrolled hypertension have detrimental effects on both the ejection fraction (EF) and LV contractile response to stress. Hypertensive LV hypertrophy has some common characteristics, including preserved global LV systolic function and LV volume with heart failure with preserved EF (HFPEF), which makes it difficult to differentiate between the two conditions at rest. Studies suggest that adopting an efficient antihypertensive therapy regimen may positively effect on the LV contractile capability in patients with long-standing hypertension. Evaluation of quantitative LV contractility under stress may be beneficial to differentiate between the hypertensive LV hypertrophy and HFPEF. It may also assist in developing a more effective modality in medical management of patients with hypertensive heart disease.

Could early septal involvement in the remodeling process be related to the advance hypertensive heart disease

Background Quantitative imaging analyses showed an earlier septal wall involvement in hypertension. We planned to determine the effect of hypertension on regional myocardial performance index (MPI) in a hypertensive patient population. Methods We evaluated 119 hypertensive patients who were divided into gr. I: 57 patients without left ventricular hypertrophy (LVH), (53.1 ± 10 years), and gr. II: 62 patients with LVH (55.1 ± 9 years) using conventional and tissue doppler imaging. They were compared with gr. III, a sex-age-matched normal control group (37 subjects, 53.0 ± 10 years). Results We detected basal septal and basal lateral contraction time (CT), isovolumetric CT and relaxation time (IVRT) and MPI. EF was 68 ± 5 % in gr. I, 69 ± 5 % in gr. II, 69 ± 4 % in gr. III. LV mass index was 122 ± 11 g/m2 in gr. I, 148 ± 13 g/m2 in gr. II and 118 ± 13 g/m2 in gr. III. Concentric LVH was detected in gr. II (relative wall thickness = 0.49 ± 0.8). LV septal and lateral MPI were abnormal in both hypertensive groups (p < 0.0001). Septal MPI was correlated moderately with septal wall thickness (r = 0.447, p < 0.001). Conclusions LV diastolic dysfunction becomes more severe in septal wall than lateral wall in hypertensive LVH. Septal myocardial performance is more dominantly affected by hypertension possibly due to earlier septal involvement in disease course. Septal MPI is correlated moderately with septal wall thickness.

Can quantitative regional myocardial dynamics contribute to the differential diagnosis of acute stress cardiomyopathy

Acute stress-induced cardiomyopathy has excessive sympathetic stimulation, microvascular dysfunction similar to hypertension. Regional prominence of left ventricular (LV) septal base and stress-induced LV hypercontractility are the particular features of both acute and chronic stress-related conditions. Novel imaging methods have shown that stress-induced cavity dilation and myocardial wall abnormalities can be a reflection of underlying previous exaggerated hypertensive episodes due to sympathetic overdrive, which results in microvascular dysfunction. Hypertension-mediated chronic stress due to increased after load episodes is possibly the main reason for blunted LV myocardial wall motion capability in patients with stress-related exaggerated hypertension. In this short report, we discussed the interrelation of myocardial dynamics and stress-induced exaggerated hypertension episodes. In addition, quantitative echocardiographic methods which previously were used for description of particular features including LV regional dynamics in hypertensive heart disease can be an option in differential diagnosis of potential cases of acute stress-induced cardiomyopathy.

Correction to: Comparison of two software systems for quantification of myocardial blood flow in patients with hypertrophic cardiomyopathy

The following information is missing from the Funding footnote on the first page of the published article: “This study was partly funded by NIH RO1 HL092985.” The last/corresponding author is incorrectly listed on the first page of the published article: The correct name is Abraham MR.

Complete reverse remodeling in acute stress cardiomyopathy. Is preserved tissue contractility under stress related to reverse remodeling

Acute stress cardiomyopathy is the unique disease which represents exaggerated and dysfunctional regions of the same cardiac tissue at the same episode. The impressive clinical course which involves the specific region is the stress-mediated exaggerated function of LV base under acutely developed stress induction. After abolishment of stress induction, dysfunctional part of LV which is the midapical myocardium undergoes a complete tissue functional recovery. The evolution of reverse remodeling in acute stress cardiomyopathy has been described using 2 and 3-dimensional echocardiography in the literature. This is the second report regarding reverse LV remodeling in acute stress cardiomyopathy in which we rather evaluate the underlying mechanisms leading complete reverse LV remodeling of dysfunctional myocardium. Therefore, we focus on the existence of preserved and exaggerated regional tissue under stress which possibly represents the predicted myocardial tissue recovery in this acute clinical entity. We also discuss the potential contribution of short-term disease course and lack of prior disease episodes to complete reverse remodeling differently from the heavy burden of chronic diseases leading to permanent tissue jeopardy.