Preheart failure comorbidities and impact on prognosis in heart failure patients: a nationwide study.

BACKGROUND: Data regarding the impact of preheart failure (HF) comorbidities on the prognosis of HF are scarce, especially in the younger HF patients. OBJECTIVES: To investigate pre-existing comorbidities in HF patients versus matched controls and to assess their impact on mortality. METHODS: We included all first-time in-hospital and outpatient diagnoses of HF from 1995 to 2017, and comorbidities antedating the HF-diagnosis in the Danish nationwide registries. HF patients were matched with up to five controls. One-year all-cause mortality rates and population attributable risk (PAR) were estimated for three separate age groups (≤50, 51-74 and >74 years). RESULTS: Totally 280 002 patients with HF and 1 166 773 controls were included. Cardiovascular comorbidities, for example, cerebrovascular disease and ischaemic heart disease were more frequent in the oldest (17.9% and 29.7% in HF vs. 9.8% and 10.7% in controls) compared to the youngest age group (3.9% and 15.2% in HF vs. 0.7% and 0.9% in controls). Amongst patients with HF, 1-year mortality rates (per 100 person-years) were highest amongst those with >1 noncardiovascular comorbidity: ≤50 years (10.4; 9.64-11.3), 51-74 years (23.3; 22.9-23.7), >74 years (58.5; 57.9-59.0); hazard ratios 245.18 (141.45-424.76), 45.85 (42.77-49.15) and 24.5 (23.64-25.68) for those ≤50, 51-74 and >74 years, respectively. For HF patients ≤50 years, PAR was greatest for hypertension (17.8%), cancer (14.1%) and alcohol abuse (8.5%). For those aged >74 years, PAR was greatest for hypertension (23.6%), cerebrovascular disease (6.2%) and cancer (7.2%). CONCLUSIONS: Heart failure patients had a higher burden of pre-existing comorbidities, compared to controls, which adversely impacted prognosis, especially in the young.

Effect of Temperature and BASF 13 338 on the Lipid Composition and Respiration of Wheat Roots.

The fatty acid composition of wheat seedling roots changed in response to temperature. As temperature declined, the level of linolenic acid increased and the level of linoleic acid decreased. The distribution of phospholipid classes was not influenced by temperature. Phosphatidyl choline and phosphatidyl ethanolamine were the predominant phospholipids isolated and comprised 85% of the total lipid phosphorus. Smaller quantities of phosphatidyl glycerol, phosphatidyl inositol, phosphatidic acid, and phosphatidyl serine were isolated. The fatty acid composition of phosphatidyl choline and phosphatidyl ethanolamine were the same and temperature affected the fatty acid composition of both phospholipids in the same manner.Growth in the presence of the substituted pyridazinone, BASF 13 338 (4-chloro-5-dimethylamino-2-phenyl-3(2H)pyridazinone), reduced the level of linolenic acid and increased the level of linoleic acid in the phosphatidyl choline, phosphatidyl ethanolamine, and total polar lipid fractions. BASF 13 338 did not affect the levels of palmitate, stearate, and oleate or the distribution of phospholipid classes.Respiration rates of wheat root tips were measured over a range of temperatures. The respiration rate declined as the temperature decreased. Neither the temperature at which the tissue was grown nor BASF 13 338 treatment influenced the ability of root tips to respire at any temperature from 4 to 30 C. The results indicated that the relative proportion of linolenic acid to linoleic acid did not influence the plants ability to grow and respire over the range of temperatures tested.

Two light sources differentially affected ferric iron reduction and growth of cotton.

In growth chambers, low pressure sodium (LPS) plus incandescent (Inc) lamps and fluorescent cool-white (FCW) plus Inc lamps were used to determine their effects on growth of cotton (Gossypium hirsutum L.) and on the reduction of Fe(3+) to Fe(2+). Cotton plants grown under LPS + Inc light developed chlorosis and grew poorly, whereas plants grown under FCW + Inc lights were green. The chlorophyll concentration and top and root weights of cotton grown under LPS + Inc were lower than those under FCW + Inc. In solution, FCW + Inc lamps reduced about eight times more Fe(3+) to Fe(2+) than did LPS + Inc lamps. Fe(3+) is transported to plant tops as Fe(3+) citrate and if we assume that FCW + Inc light reduces Fe(3+) to Fe(2+) in plant foliage as it did in the solutions, then reduction of Fe(3+) by the light environment will make Fe(2+) in the tops more available for biochemical reactions.

Inhibition of linolenic Acid synthesis and modification of chilling resistance in cotton seedlings.

The temperature at which cotton seeds (Gossypium hirsutum L.) germinated influenced the fatty acid composition of the polar lipids of developing root tips. Seeds were germinated at 15, 20, 25, and 30 C. As the temperature decreased the linolemic acid content of the polar lipid fraction increased. Sandoz 9785[4-chloro-5-(dimethylamino)-2-phenyl-3(2H)-pyridazinone] reduced the low temperature-induced increase in linolenic acid content of the polar lipids and reduced seedling ability to withstand 8 C chilling. The results are consistent with the conclusion that chilling resistance in cotton seedlings is related to the level of linolenic acid in the polar lipids in the developing root tips.

Interactions of lipoidal materials and a pyridazinone inhibitor of chloroplast development.

Formation of chloroplast pigments was inhibited, and free fatty acids accumulated in mustard (Brassica juncea [L.] Coss.) cotyledons and in barley (Hordeum vulgare L.) first leaves developed after treatment with 4-chloro-5- (dimethylamino)-2- (alpha, alpha, alpha-trifluoro-m-tolyl) -3 (2H) -pyridazinone. The inhibitor reduced the amount of fatty acids found in polar lipids (galactolipids) of barley chloroplasts and increased the amount in nonpolar lipids while having little effect on total content of bound fatty acids. The inhibition of chlorophyll formation was circumvented by D-alpha-tocopherol acetate, phytol, farnesol, and squalene, and by unsaturated fatty acids and their methyl esters. The protective action can be explained partially by an interaction external to the plant whereby 4-chloro-5- (dimethylamino) -2- (alpha, alpha, alpha-trifluoro-m-tolyl) -3 (2H) -pyridazinone partitioned out of the aqueous phase and into the lipid phase, thus limiting availability of the inhibitor to plants. However, the amount of inhibitor reaching the cotyledons of tocopherol-protected mustard seedlngs was still in excess of the amount necessary to cause white foliage, but it failed to produce the effect. Tocopherol treatment did not prevent the 4-chloro-5- (dimethylamino) -2- (alpha, alpha, alpha-trifluoro-m-tolyl) -3 (2H) -pyridazinone-induced buildup of fatty acids in mustard cotyledons but did partially circumvent the effect in barley leaves. The amount of linolenic acid relative to linoleic acid was reduced in barley leaves and chloroplasts by 4-chloro-5- (dimethylamino) -2- (alpha, alpha, alpha-trifluoro-m-tolyl) -3 (2H) -pyridazinone action and this effect was circumvented by tocopherol.

Stimulation of Solute Loss from Radicles of Gossypium hirsutum L. by Chilling, Anaerobiosis, and Low pH.

The loss of organic substances from cotton (Gossypium hirsutum L.) radicles is enhanced by chilling, low pH, or anaerobic conditions. Solute loss returns to a low level when the stimulus is removed, indicating no permanent injury to membranes. Loss of solute induced by chilling or anaerobiosis is reversed or prevented by calcium or magnesium. These cations did not reduce the solute loss resulting from low pH. The site of loss appears to be localized at or near the root tip. If the seedling cotyledons are removed, the loss is greatly reduced, indicating the need for a reserve pool of organic substances.

Induction and prevention of chilling injury to radicle tips of imbibing cottonseed.

Cottonseed exposed to a temperature of 5 degrees during hydration are killed, or the subsequent germination performance of surviving seed is seriously inhibited. Exposure to chilling for periods as short as 30 minutes reduces germination speed and induces root abnormalities, while chilling for 12 hours may kill all seed. Sensitivity to chilling persists during the initial 2 to 4 hours of hydration. Seeds imbibed 4 hours at 31 degrees , then dried, retain immunity to chilling. An irreversible event that is blocked or disrupted by chilling apparently occurs during early seed hydration.

Periods of sensitivity to chilling in germinating cotton.

Cotton seedlings were subjected to a 96 hour chilling treatment (5 degrees or 10 degrees ) after periods of germination at 31 degrees ranging from 0 to 48 hours. Inhibition of subsequent growth at a favorable temperature by chilling was dependent on level of low temperature and stage of seedling development when chilled. Two periods of chilling hypersensitivity were observed during germination: 1) coincident with subjection of seed to a germination environment; and 2) after 18 to 30 hours of germination at 31 degrees . Subsequent growth of seedlings chilled after 12 to 18 hours or 48 hours of germination at 31 degrees was relatively unaffected. It is suggested that chilling alters specifically timed events that occur at the initiation of germination and after 18 to 30 hours of germination, and that alteration of these germination processes is visited on long term subsequent growth of the plant.